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Does Albutrepenonacog alfa and Aceclofenac interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Aceclofenac may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Acemetacin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Acemetacin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Acenocoumarol interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Acenocoumarol, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Acetaminophen interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Acetaminophen may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Acetazolamide interact?
null
The subject drug induces diuresis1,2, which can theoretically increase the excretion rate of the affected drug, which is eliminated by the kidneys. Additionally, it could affect renal tubular reabsorption of certain drugs. Exposure to the affected drug can be markedly reduced, leading to subtherapeutic drug levels that are unlikely to elicit an adequate clinical response. In short, Acetazolamide may increase the excretion rate of Albutrepenonacog alfa which could result in a lower serum level and potentially a reduction in efficacy, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Acetylsalicylic acid interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Acetylsalicylic acid may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Aclidinium interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Aclidinium may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Acyclovir interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Acyclovir may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Adefovir dipivoxil interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Adefovir dipivoxil may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Aldesleukin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Aldesleukin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Allopurinol interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Allopurinol may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Almotriptan interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Almotriptan may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Alogliptin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Alogliptin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Alpha-1-proteinase inhibitor interact?
null
Antifibrinolytic agents prevent the breakdown of blood clots or thrombus. Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. Co-administration of an antifibrinolytic agent and blood coagulation factor may result in an additive thrombogenic effect and an increased risk of acquiring thrombotic disorders, such as pulmonary embolism, venous thrombosis, and arterial thrombosis. In short, Alpha-1-proteinase inhibitor may increase the thrombogenic activities of Albutrepenonacog alfa, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Alprazolam interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Alprazolam may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Alteplase interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, anticoagulant drugs serve to prevent or reduce blood coagulation or prolong the clotting time. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of anticoagulant agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Alteplase, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Amantadine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Amantadine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Amikacin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. The affected drug is a narrow therapeutic index drug that undergoes renal excretion as its main elimination pathway: a change in serum concentration may significantly elevate the risk of developing drug-related adverse effects. In short, Albutrepenonacog alfa may decrease the excretion rate of Amikacin which could result in a higher serum level, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Amiloride interact?
null
The subject drug induces diuresis1,2, which can theoretically increase the excretion rate of the affected drug, which is eliminated by the kidneys. Additionally, it could affect renal tubular reabsorption of certain drugs. Exposure to the affected drug can be markedly reduced, leading to subtherapeutic drug levels that are unlikely to elicit an adequate clinical response. In short, Amiloride may increase the excretion rate of Albutrepenonacog alfa which could result in a lower serum level and potentially a reduction in efficacy, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Aminocaproic acid interact?
null
The administration of aminocaproic acid with other agents capable of inducing coagulation, such as the affected drug, may increase the risk of thrombosis. Evidence is conflicting - there exists some evidence that this combination of agents does not initiate the coagulation cascade, does not present risk of thrombosis, and may be safe and effective. In contrast, case reports exist of this combination of agents resulting in thrombosis, and prescribing information for aminocaproic acid warns of this interaction. This interaction is likely due to an additive pharmacodynamic effect between multiple agents capable of inducing coagulation. In short, The risk or severity of adverse effects can be increased when Aminocaproic acid is combined with Albutrepenonacog alfa, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Amitriptyline interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Amitriptyline may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ammonium chloride interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Ammonium chloride may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Amoxicillin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Amoxicillin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Amphetamine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Amphetamine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Amphotericin B interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Amphotericin B may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ampicillin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Ampicillin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Antihemophilic factor (recombinant), PEGylated interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Antihemophilic factor (recombinant), PEGylated may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Antipyrine interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Antipyrine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Antithrombin Alfa interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Antithrombin Alfa, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Antithrombin III human interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Antithrombin III human, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Apalutamide interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Apalutamide may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Apixaban interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Apixaban, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Apremilast interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Apremilast may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Aprotinin interact?
null
Antifibrinolytic agents prevent the breakdown of blood clots or thrombus. Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. Co-administration of an antifibrinolytic agent and blood coagulation factor may result in an additive thrombogenic effect and an increased risk of acquiring thrombotic disorders, such as pulmonary embolism, venous thrombosis, and arterial thrombosis. In short, Aprotinin may increase the thrombogenic activities of Albutrepenonacog alfa, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Arformoterol interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Arformoterol may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Argatroban interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Argatroban, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Arsenic trioxide interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Arsenic trioxide may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Atazanavir interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Atazanavir may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Atomoxetine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Atomoxetine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Auranofin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Auranofin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Azacitidine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Azacitidine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Azathioprine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Azathioprine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Azelaic acid interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Azelaic acid may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Aztreonam interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Aztreonam may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bacitracin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Bacitracin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Baclofen interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Baclofen may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Balsalazide interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Balsalazide may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Baricitinib interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Baricitinib may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bemiparin interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Bemiparin, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Benzatropine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Benzatropine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Benznidazole interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Benznidazole may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Benzydamine interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Benzydamine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bepotastine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bepotastine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Betrixaban interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Betrixaban, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Bicisate interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bicisate may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bismuth subgallate interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Albutrepenonacog alfa may decrease the excretion rate of Bismuth subgallate which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bisoprolol interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bisoprolol may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bivalirudin interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Bivalirudin, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Bleomycin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bleomycin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Brivaracetam interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Brivaracetam may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bromazepam interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bromazepam may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bromotheophylline interact?
null
The subject drug induces diuresis1,2, which can theoretically increase the excretion rate of the affected drug, which is eliminated by the kidneys. Additionally, it could affect renal tubular reabsorption of certain drugs. Exposure to the affected drug can be markedly reduced, leading to subtherapeutic drug levels that are unlikely to elicit an adequate clinical response. In short, Bromotheophylline may increase the excretion rate of Albutrepenonacog alfa which could result in a lower serum level and potentially a reduction in efficacy, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Budesonide interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Budesonide may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Bumetanide interact?
null
The subject drug induces diuresis1,2, which can theoretically increase the excretion rate of the affected drug, which is eliminated by the kidneys. Additionally, it could affect renal tubular reabsorption of certain drugs. Exposure to the affected drug can be markedly reduced, leading to subtherapeutic drug levels that are unlikely to elicit an adequate clinical response. In short, Bumetanide may increase the excretion rate of Albutrepenonacog alfa which could result in a lower serum level and potentially a reduction in efficacy, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Bupropion interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Bupropion may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Buspirone interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Buspirone may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Canagliflozin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Canagliflozin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cangrelor interact?
null
Blood coagulation factors promote the blood coagulation pathways to ultimately form the insoluble fibrin clot. In contrast, fibrinolytic agents activate the fibrinolytic system by conversion of the inactive proenzyme, plasminogen into the active enzyme plasmin, that degrades fibrin to break down the insoluble clot [A38173]. Desired procoagulant effects of blood coagulation factors may be reduced with the combination use of fibrinolytic agents. In short, The therapeutic efficacy of Albutrepenonacog alfa can be decreased when used in combination with Cangrelor, and the severity of the interaction is major.
Does Albutrepenonacog alfa and Canrenoic acid interact?
null
The subject drug induces diuresis1,2, which can theoretically increase the excretion rate of the affected drug, which is eliminated by the kidneys. Additionally, it could affect renal tubular reabsorption of certain drugs. Exposure to the affected drug can be markedly reduced, leading to subtherapeutic drug levels that are unlikely to elicit an adequate clinical response. In short, Canrenoic acid may increase the excretion rate of Albutrepenonacog alfa which could result in a lower serum level and potentially a reduction in efficacy, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Capecitabine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Capecitabine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Capreomycin interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. The affected drug is a narrow therapeutic index drug that undergoes renal excretion as its main elimination pathway: a change in serum concentration may significantly elevate the risk of developing drug-related adverse effects. In short, Albutrepenonacog alfa may decrease the excretion rate of Capreomycin which could result in a higher serum level, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Carbamazepine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. The affected drug is a narrow therapeutic index drug that undergoes renal excretion as its main elimination pathway: a change in serum concentration may significantly elevate the risk of developing drug-related adverse effects. In short, Albutrepenonacog alfa may decrease the excretion rate of Carbamazepine which could result in a higher serum level, and the severity of the interaction is moderate.
Does Albutrepenonacog alfa and Carbidopa interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Carbidopa may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Carboplatin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Carboplatin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Carmustine interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Carmustine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefaclor interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefaclor may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefadroxil interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefadroxil may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefalotin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefalotin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefapirin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefapirin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefazolin interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefazolin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefdinir interact?
null
The renal excretion of drugs is the overall result of a combination of kidney processes that include glomerular filtration, passive diffusion, tubular secretion, and tubular reabsorption. Since two of these mechanisms - tubular secretion and reabsorption - are saturable processes , they are consequently susceptible to competition between multiple substrates excreted by the kidneys. If two or more medications that are mainly renally excreted are co-administered, they may compete for renal elimination; there is a large likelihood that one agent may "out-compete" or saturate the renal excretion mechanisms before the other concomitantly administered agent(s) are excreted. As a result, the elimination of these other concurrently administered agents may be inhibited or otherwise delayed, which could lead to increases in their serum concentrations and the risk, incidence, and/or severity of adverse effects associated with the exposure to such drugs. In short, Cefdinir may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefditoren interact?
null
The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefditoren may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefepime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefepime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefmetazole interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefmetazole may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefoperazone interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefoperazone may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefotaxime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefotaxime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefotetan interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefotetan may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefotiam interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefotiam may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefoxitin interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefoxitin may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefpirome interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefpirome may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefpodoxime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefpodoxime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefprozil interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefprozil may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefradine interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefradine may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftaroline fosamil interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftaroline fosamil may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftazidime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftazidime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftibuten interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftibuten may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftizoxime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftizoxime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftobiprole interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftobiprole may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Ceftriaxone interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Ceftriaxone may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.
Does Albutrepenonacog alfa and Cefuroxime interact?
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The subject drug is a nephrotoxic agent that may potentially impair renal function and decrease the excretion of drugs that mainly undergo renal excretion as the principal mode of clearance, such as the affected drug. Attenuated renal excretion of the affected drug may increase drug concentrations, leading to an elevated risk for drug-related adverse effects. In short, Cefuroxime may decrease the excretion rate of Albutrepenonacog alfa which could result in a higher serum level, and the severity of the interaction is minor.