Pralsetinib

Research use only, not for human use.

Pralsetinib (BLU-667) is a highly potent, selective RET inhibitor (IC50s: 0.4, 0.3, 0.4, 0.4, and 0.4 nM for WT RET, RET mutants V804L, V804M, M918T and CCDC6-RET fusion).

Pralsetinib (BLU-667) is a highly potent, selective RET inhibitor (IC50s: 0.4, 0.3, 0.4, 0.4, and 0.4 nM for WT RET, RET mutants V804L, V804M, M918T and CCDC6-RET fusion).Pralsetinib demonstrates more than 10-fold increased potency over approved MKIs against oncogenic RET variants and resistance mutants. Pralsetinib demonstrates potent activity (IC50: 0.4 nM) against common oncogenic RET alterations, including RET M918T, an activating mutation found in MTC, as well as the CCDC6-RET fusion observed in PTC and NSCLC. Pralsetinib suppresses RET pathway signaling in a panel of RET-driven cell lines: LC2/ad (CCDC6-RET, NSCLC), MZ-CRC-1 (RET M918T, MTC), and TT (RET C634W, MTC).Pralsetinib potently inhibits the growth of NSCLC and thyroid cancer xenografts driven by various RET mutations and fusions without inhibiting VEGFR-2. Pralsetinib shows dose-dependent activity against both KIF5B-RET Ba/F3 and KIF5B-RET V804L Ba/F3 allograft tumors with doses as low as 10 mg/kg twice daily.(In Vitro):Pralsetinib (BLU-667) demonstrates more than 10-fold increased potency over approved MKIs against oncogenic RET variants and resistance mutants.Pralsetinib (BLU-667) demonstrates potent activity (IC50=0.4 nM) against common oncogenic RET alterations, including RET M918T, an activating mutation found in MTC, as well as the CCDC6-RET fusion observed in PTC and NSCLC. Pralsetinib (BLU-667) suppresses RET pathway signaling in a panel of RET-driven cell lines: LC2/ad (CCDC6-RET, NSCLC), MZ-CRC-1 (RET M918T, MTC), and TT (RET C634W, MTC).(In Vivo):Pralsetinib (BLU-667) potently inhibits growth of NSCLC and thyroid cancer xenografts driven by various RET mutations and fusions without inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2).Pralsetinib (BLU-667) shows dose dependent activity against both KIF5B-RET Ba/F3 and KIF5B-RET V804L Ba/F3 allograft tumors with doses as low as 10 mg/kg twice-daily.

Pralsetinib (BLU-667) demonstrates more than 10-fold increased potency over approved MKIs against oncogenic RET variants and resistance mutants. ?Pralsetinib (BLU-667) demonstrates potent activity (IC50=0.4 nM) against common oncogenic RET alterations, including RET M918T, an activating mutation found in MTC, as well as the CCDC6-RET fusion observed in PTC and NSCLC. ?Pralsetinib (BLU-667) suppresses RET pathway signaling in a panel of RET-driven cell lines: LC2/ad (CCDC6-RET, NSCLC), MZ-CRC-1 (RET M918T, MTC), and TT (RET C634W, MTC).

Pralsetinib (BLU-667) potently inhibits growth of NSCLC and thyroid cancer xenografts driven by various RET mutations and fusions without inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2).Pralsetinib (BLU-667) shows dose dependent activity against both KIF5B-RET Ba/F3 and KIF5B-RET V804L Ba/F3 allograft tumors with doses as low as 10 mg/kg twice-daily.

Blu667

Tyrosine Kinase

c-RET

RET

Cancer

Solid tumours

2097132-94-8

533.6

C27H30FN9O2

>98% (HPLC)

DMSO:95 mg/mL (178.04 mM)

COC1(CCC(CC1)C1=NC(C)=CC(NC2=NNC(C)=C2)=N1)C(=O)N[C@@H](C)C1=CN=C(C=C1)N1C=C(F)C=N1

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(-20℃)

With Ice Pack

≥ 2 years