Can you take Nubeqa with Vimseltinib?

Vimseltinib has a moderate potential interaction with Biliary Obstruction.

Vimseltinib should be avoided in patients with preexisting increased serum transaminases; total bilirubin or direct bilirubin (greater than 1 times the upper limit of normal [1 x ULN]); or active liver or biliary tract disease, including alkaline phosphatase. Liver tests (including AST, ALT, total bilirubin, direct bilirubin, alkaline phosphatase, and GGT) should be monitored before starting vimseltinib, twice a month for the first 2 months of therapy, every 3 months for the first year of therapy, and as clinically indicated thereafter. Vimseltinib has not been studied in patients with moderate (bilirubin greater than 1.5 to 3 x ULN and any AST) or severe (bilirubin greater than 3 x ULN and any AST) liver dysfunction. No dose adjustment is recommended for patients with mild (bilirubin up to 1 x ULN and AST greater than 1 x ULN or bilirubin greater than 1 to 1.5 x ULN and any AST) liver dysfunction.

Vimseltinib has a moderate potential interaction with Hyperbilirubinemia.

Vimseltinib should be avoided in patients with preexisting increased serum transaminases; total bilirubin or direct bilirubin (greater than 1 times the upper limit of normal [1 x ULN]); or active liver or biliary tract disease, including alkaline phosphatase. Liver tests (including AST, ALT, total bilirubin, direct bilirubin, alkaline phosphatase, and GGT) should be monitored before starting vimseltinib, twice a month for the first 2 months of therapy, every 3 months for the first year of therapy, and as clinically indicated thereafter. Vimseltinib has not been studied in patients with moderate (bilirubin greater than 1.5 to 3 x ULN and any AST) or severe (bilirubin greater than 3 x ULN and any AST) liver dysfunction. No dose adjustment is recommended for patients with mild (bilirubin up to 1 x ULN and AST greater than 1 x ULN or bilirubin greater than 1 to 1.5 x ULN and any AST) liver dysfunction.

The darolutamide in Nubeqa has a moderate potential interaction with Liver Disease.

Patients with moderate hepatic impairment (Child-Pugh Class B) have a higher exposure to darolutamide and reduction of the dose is recommended (see manufacturer package insert for recommended dose). No dose reduction is needed for patients with mild hepatic impairment. The effect of severe hepatic impairment (Child-Pugh C) on darolutamide pharmacokinetics is unknown.

Vimseltinib has a moderate potential interaction with Liver Disease.

Vimseltinib should be avoided in patients with preexisting increased serum transaminases; total bilirubin or direct bilirubin (greater than 1 times the upper limit of normal [1 x ULN]); or active liver or biliary tract disease, including alkaline phosphatase. Liver tests (including AST, ALT, total bilirubin, direct bilirubin, alkaline phosphatase, and GGT) should be monitored before starting vimseltinib, twice a month for the first 2 months of therapy, every 3 months for the first year of therapy, and as clinically indicated thereafter. Vimseltinib has not been studied in patients with moderate (bilirubin greater than 1.5 to 3 x ULN and any AST) or severe (bilirubin greater than 3 x ULN and any AST) liver dysfunction. No dose adjustment is recommended for patients with mild (bilirubin up to 1 x ULN and AST greater than 1 x ULN or bilirubin greater than 1 to 1.5 x ULN and any AST) liver dysfunction.

The darolutamide in Nubeqa has a moderate potential interaction with Renal Dysfunction.

Patients with severe renal impairment (eGFR 15-29 mL/min/1.73 m2) who are not receiving hemodialysis have a higher exposure to darolutamide and reduction of the dose is recommended (see manufacturer package insert for recommended dose). No dose reduction is needed for patients with mild or moderate renal impairment. The effect of end stage renal disease (eGFR <15 mL/min/1.73 m2) on darolutamide pharmacokinetics is unknown.

Vimseltinib has a moderate potential interaction with Renal Dysfunction.

During vimseltinib treatment, renal function should be assessed using alternative measures that are not based on serum creatinine. In 1 study, serum creatinine increased by a mean of 19 mcmol/L compared to baseline. These increases in serum creatinine may not be associated with changes in renal function but may be due to inhibition of renal tubular secretion transporters. Creatinine increases reversed when vimseltinib was discontinued. The effect of severe renal dysfunction (estimated GFR less than 30 mL/min) on vimseltinib pharmacokinetics is unknown.