DelveInsight has recently published a report on “TRUSELTIQ Market Forecast Report” providing an in-depth analysis of the TRUSELTIQ market analysis and forecasts up to 2032 in the seven major markets (7MM) (i.e. the United States, EU4 (Germany, France, Italy, and Spain), the United Kingdom, and Japan. The comprehensive report provides an analysis of TRUSELTIQ market potential and market share analysis in the Cholangiocarcinoma therapeutics space across the 7MM from 2019 to 2032.
The report also helps you to understand the TRUSELTIQ clinical and commercial developments along with parameters like the drug’s Mechanism of Action (MOA), Route of Administration (ROA), dosage, and special designations.
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TRUSELTIQ Drug Summary
TRUSELTIQ (infigratinib) is an orally administered FGFR1-3 tyrosine kinase inhibitor in development for the treatment of patients with FGFR-driven diseases, including cholangiocarcinoma (bile duct cancer), urothelial carcinoma (bladder cancer), and achondroplasia. Infigratinib sparingly inhibits FGFR4; patients may tolerate it better than pan-FGFR1-4 inhibitors. QED Therapeutics holds worldwide rights to infigratinib to evaluate its safety and efficacy for multiple FGFR-driven diseases.
The company is also evaluating the product in a phase III clinical study for first-line therapy for cholangiocarcinoma (bile duct cancer) and in a phase II as second-line therapy for cholangiocarcinoma (bile duct cancer). It presented data on infigratinib in cholangiocarcinoma and urothelial carcinoma at the American Society of Clinical Oncology 2020 virtual scientific program.
Dosage and administration
The recommended dosage of TRUSELTIQ is 125 mg (one 100 mg capsule and one 25 mg capsule) taken orally once daily for 21 consecutive days followed by 7 days off therapy, in 28-day cycles. Continue treatment until disease progression or unacceptable toxicity
If a dose of TRUSELTIQ is missed by ≥4 hours or if vomiting occurs, instruct patients to resume the regular daily dose schedule for TRUSELTIQ the next day.
Mechanism of Action
Infigratinib is a small-molecule kinase inhibitor of FGFR with IC50 values of 1.1, 1, 2, and 61 nM for FGFR1, FGFR2, FGFR3, and FGFR4, respectively. The major human metabolites of infigratinib, BHS697 and CQM157, have similar in vitro binding affinities for FGFR1, FGFR2, and FGFR3 compared to infigratinib. Infigratinib inhibited FGFR signaling and decreased cell proliferation in cancer cell lines with activating FGFR amplifications, mutations, or fusions. Constitutive FGFR signaling can support the proliferation and survival of malignant cells. Infigratinib had anti-tumor activity in mouse and rat xenograft models of human tumors with activating FGFR2 or FGFR3 alterations, including two patient-derived xenograft models of cholangiocarcinoma that expressed FGFR2-TTC28 or FGFR2-TRA2B fusions. Infigratinib demonstrated brain-to-plasma concentration ratios (based on AUC0-inf) of 0.682 in rats after a single oral dose.
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