Can you take Pacritinib with Sodium phenylbutyrate / taurursodiol?

Pacritinib has a moderate potential interaction with Arrhythmia.

Pacritinib can cause a QT prolongation of greater than 500 msec, and patients receiving this drug were more likely to develop a QT prolongation of at least 60 msec from baseline (compared to the control group) in clinical trials. This agent should be avoided in patients with QT intervals greater than 480 msec at baseline, and/or in those who are taking medications known to prolong the QTc interval. Hypokalemia should be corrected before initiating and during therapy with this agent. QT prolongation occurring during treatment should be managed with treatment interruption and electrolyte management. Periodic monitoring of ECGs and electrolytes is recommended in these patients.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Biliary Obstruction.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

Pacritinib has a moderate potential interaction with Bleeding Associated with Coagulation Defect.

Serious episodes of bleeding, including those requiring transfusion/invasive intervention, and some leading to fatal bleeding events have been reported in patients treated with pacritinib. Platelet counts should be periodically assessed, monitoring for signs of bleeding (when indicated); hemorrhage should be managed with medical intervention, dose reductions, intermittent interruptions, and/or permanent treatment discontinuations. It is recommended to withhold pacritinib for 7 days prior to planned surgery/invasive procedure.

Pacritinib has a moderate potential interaction with Bleeding Disorder.

Serious episodes of bleeding, including those requiring transfusion/invasive intervention, and some leading to fatal bleeding events have been reported in patients treated with pacritinib. Platelet counts should be periodically assessed, monitoring for signs of bleeding (when indicated); hemorrhage should be managed with medical intervention, dose reductions, intermittent interruptions, and/or permanent treatment discontinuations. It is recommended to withhold pacritinib for 7 days prior to planned surgery/invasive procedure.

Pacritinib has a major potential interaction with Cardiovascular Conditions and Disorders.

In a major safety study of a Janus kinase (JAK) inhibitor, tofacitinib, in rheumatoid arthritis patients 50 years and older with at least 1 cardiovascular risk factor, higher rates of all-cause mortality (including sudden cardiovascular death) and major adverse cardiovascular events (MACE) (defined as cardiovascular death, myocardial infarction, and stroke) were observed with the JAK inhibitor when compared with tumor necrosis factor (TNF) blockers. Patients who were current or past smokers had an additional increased risk. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including baricitinib, upadacitinib, ruxolitinib, fedratinib, ritlecitinib, deuruxolitinib, and pacritinib. Consider the benefits and risks for each individual patient prior and during treatment with JAK inhibitors, especially in patients with other cardiovascular risk factors, history of cardiovascular events, and patients who are current or past smokers. Patients should be informed about the symptoms of serious cardiovascular events and what to do if they occur.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Central Nervous System Disorders.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

Pacritinib has a major potential interaction with Diarrhea.

Severe diarrhea, sometimes requiring discontinuation of treatment, has occurred in patients treated with pacritinib. Preexisting diarrhea should be controlled prior to starting treatment with pacritinib. Antidiarrheal agents should be promptly used to treat diarrhea at the first onset of symptoms. Antidiarrheal agents, fluid replacement, and/or dose modification should be used to manage diarrhea. Reducing or interrupting pacritinib should be considered in patients with significant diarrhea (despite optimal supportive care).

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Fluid Retention.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Gallbladder Disease.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Heart Failure.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

Pacritinib has a major potential interaction with Infection.

Serious and sometimes fatal infections due to bacterial, mycobacterial, invasive fungal, viral, or other opportunistic pathogens have been reported in patients receiving pacritinib. It is recommended to avoid the use of pacritinib in patients with an active, serious infection, including localized infections and to consider the risks and benefits before starting treatment. Patients should be closely monitored for the development of signs and symptoms of infection during and after treatment. Treatment should be interrupted if a patient develops a serious infection, an opportunistic infection, or sepsis and appropriate therapy should be instituted according to clinical guidelines. Close monitoring is recommended.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Liver Disease.

Sodium phenylbutyrate is primarily metabolized in the liver and kidney. Therapy with sodium phenylbutyrate should be administered cautiously in patients with liver disease. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

The taurursodiol in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Malabsorption Syndrome.

Sodium phenylbutyrate-taurursodiol contains taurursodiol, a bile acid. In patients with disorders that interfere with bile acid circulation, there may be an increased risk for diarrhea and patients should be monitored appropriately. Other conditions such as pancreatic insufficiency, intestinal malabsorption, or intestinal diseases that may alter the concentration of bile acids, may also lead to decreased absorption of this drug and its components. Consider consulting with a GI specialists with experience managing these GI disorders. Patients with disorders of enterohepatic circulation (e.g., biliary infection, active cholecystitis, etc.), severe pancreatic disorders (e.g., pancreatitis), and intestinal disorders that may alter concentrations of bile acids (e.g., ileal resection, regional ileitis, etc.) were excluded from clinical studies and there is no experience in patients with these conditions. Caution is advised.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Myoneural Disorder.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Peripheral Neuropathy.

Sodium phenylbutyrate is a pro-drug and is rapidly metabolized to the active, phenylacetate. Neurotoxicity, including exacerbation of a preexisting neuropathy, has been reported with the use of intravenous phenylacetate. The acute onset and reversibility when the phenylacetate infusion was discontinued suggested a drug effect. Care should be exercised when prescribing sodium phenylbutyrate to patients at risk for neurotoxicity.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a major potential interaction with Renal Dysfunction.

The use of sodium phenylbutyrate may cause fluid retention in patients with congestive heart failure, renal dysfunction, or sodium retention with edema. Sodium phenylbutyrate is primarily excreted by the kidney and these patients may exhibit reduced excretion. Therapy with sodium phenylbutyrate should be administered cautiously in these patients. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

The sodium phenylbutyrate in sodium phenylbutyrate / taurursodiol has a moderate potential interaction with Renal Dysfunction.

Sodium phenylbutyrate is primarily metabolized in the liver and kidney. Therapy with sodium phenylbutyrate should be administered cautiously in patients with liver disease. Monitoring plasma levels of ammonia, arginine, branched-chain amino acids and serum proteins to maintain within normal limits and glutamine to less than 1000 mcmol/L is recommended.

Pacritinib has a major potential interaction with Smoking.

In a major safety study of a Janus kinase (JAK) inhibitor, tofacitinib, in rheumatoid arthritis patients 50 years and older with at least 1 cardiovascular risk factor, higher rates of all-cause mortality (including sudden cardiovascular death) and major adverse cardiovascular events (MACE) (defined as cardiovascular death, myocardial infarction, and stroke) were observed with the JAK inhibitor when compared with tumor necrosis factor (TNF) blockers. Patients who were current or past smokers had an additional increased risk. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including baricitinib, upadacitinib, ruxolitinib, fedratinib, ritlecitinib, deuruxolitinib, and pacritinib. Consider the benefits and risks for each individual patient prior and during treatment with JAK inhibitors, especially in patients with other cardiovascular risk factors, history of cardiovascular events, and patients who are current or past smokers. Patients should be informed about the symptoms of serious cardiovascular events and what to do if they occur.

Pacritinib has a major potential interaction with Smoking.

Malignancies (including lymphomas and solid tumors) have been reported in patients treated with tofacitinib, baricitinib, upadacitinib, deuruxolitinib and other Janus kinase (JAK) inhibitors used to treat inflammatory conditions. Patients who are current or past smokers are at additional increased risk of malignancies. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including ruxolitinib, pacritinib, and fedratinib. Before starting or continuing therapy, the benefits and risks for the individual patient should be considered, especially in patients with a known malignancy (other than successfully treated nonmelanoma skin cancer), patients who develop a malignancy during therapy, and patients who are current or past smokers. Periodic skin examination is recommended for patients who are at increased risk for skin cancer.

Pacritinib has a major potential interaction with Thrombotic/Thromboembolic Disorder.

Thrombosis (including deep venous thrombosis, pulmonary embolism, cerebral venous sinus thrombosis, and arterial thrombosis) has occurred in patients treated for inflammatory conditions with Janus kinase (JAK) inhibitors, including baricitinib, tofacitinib, deuruxolitinib and upadacitinib. Many of these adverse events were serious and some resulted in death. Based on a shared mechanism of action, this risk should be considered for other JAK inhibitors, including ruxolitinib, fedratinib, and pacritinib. In general, JAK inhibitors should be avoided in patients who may be at increased risk of thrombosis. Tofacitinib should be used at the lowest effective dose and for the shortest duration needed to achieve/maintain therapeutic response when treating ulcerative colitis. If symptoms of thrombosis occur in any patients receiving JAK inhibitors, treatment should be discontinued and patients should be evaluated promptly and treated appropriately.

Pacritinib has a moderate potential interaction with Ventricular Arrhythmia.

Pacritinib can cause a QT prolongation of greater than 500 msec, and patients receiving this drug were more likely to develop a QT prolongation of at least 60 msec from baseline (compared to the control group) in clinical trials. This agent should be avoided in patients with QT intervals greater than 480 msec at baseline, and/or in those who are taking medications known to prolong the QTc interval. Hypokalemia should be corrected before initiating and during therapy with this agent. QT prolongation occurring during treatment should be managed with treatment interruption and electrolyte management. Periodic monitoring of ECGs and electrolytes is recommended in these patients.