1416241-23-0
1416241-23-0 structure
- Name: Vamotinib
- Chemical Name: Vamotinib
- CAS Number: 1416241-23-0
- Molecular Formula: C29H27F3N6O
- Molecular Weight: 532.56
- Catalog: Signaling Pathways Protein Tyrosine Kinase/RTK c-Met/HGFR
- Create Date: 2022-10-16 18:48:25
- Modify Date: 2024-11-29 21:06:27
-
Vamotinib (PF-114) is a potent, selective and orally active tyrosine kinase inhibitor. Vamotinib inhibits the autophosphorylation of BCR/ABL and BCR/ABL-T315I. Vamotinib induces apoptosis. Vamotinib shows anti-proliferative and anti-tumor activity. Vamotinib has the potential for the research of resistant philadelphia chromosome-positive (Ph+) leukemia[1].
| Name | Vamotinib |
|---|
| Description | Vamotinib (PF-114) is a potent, selective and orally active tyrosine kinase inhibitor. Vamotinib inhibits the autophosphorylation of BCR/ABL and BCR/ABL-T315I. Vamotinib induces apoptosis. Vamotinib shows anti-proliferative and anti-tumor activity. Vamotinib has the potential for the research of resistant philadelphia chromosome-positive (Ph+) leukemia[1]. |
|---|---|
| Related Catalog | |
| In Vitro | Vamotinib (0-1 µM) inhibits ABL kinase and its mutants with IC50s of 0.49, 0.78, 1.0 µM for ABL, ABL(T315l), ABL(H396P), respectively[1]. Vamotinib (0-1000 nM) inhibits the autophosphorylation of BCR/ABL and BCR/ABL-T315I in a dose-dependent manner[1]. Vamotinib (0-2000 nM) shows anti-proliferative activity in Ba/F3 cells expressing native BCR/ABL[1]. Vamotinib (0-100 nM) induces apoptosis in Ba/F3 cells expressing BCR/ABL and BCR/ABL-T315I[1]. Vamotinib (0-1000 nM) inhibits the growth of Ph+ patient-derived cell lines in k562, kcl-22, SupB15, Tom-1, BV-173 cells[1]. Vamotinib (0-1000 nM) suppresses growth of Ph+ PD-LTC with nonmutational resistance as well as T315I mutation[1]. Western Blot Analysis[1] Cell Line: Ba/F3 cells Concentration: 0, 10, 25, 50, 100, 500, 1000 nM Incubation Time: Result: Inhibited the autophosphorylation of BCR/ABL and BCR/ABL-T315I in a dose-dependent manner and inhibited substrate phosphorylation as shown by the reduced Crkl-phosphorylation and downstream activation of Stat5 by BCR/ABL, as well as by BCR/ABL-T315I. Cell Proliferation Assay[1] Cell Line: Ba/F3 cells Concentration: 0, 50, 500, 2000 nM Incubation Time: Result: Potently inhibited proliferation of Ba/F3 cells expressing native BCR/ABL in a dose-dependent manner and shows no effects on empty vector-transduced Ba/F3 cells in the presence of IL-3 (10 ng/ml). Apoptosis Analysis[1] Cell Line: Ba/F3 cells Concentration: 0-100 nM Incubation Time: Result: Induced apoptosis in Ba/F3 cells expressing BCR/ABL and BCR/ABL-T315I in a dose dependent manner. |
| In Vivo | Vamotinib (25, 40 mg/kg; i.g.; daily for 14 consecutive days) shows anti-tumor activity[1]. Vamotinib (50 mg/kg; p.o.; once daily for 20 days) prolongs the survival of mice with both BCR/ABL- and BCR/ABL-T315I-driven CML-like disease[1]. Animal Model: Female BALB/cAnNRj-Foxn1nu mice (K562 nude mouse xenograft model)[1] Dosage: 25, 40 mg/kg Administration: Oral gavage; daily for 14 consecutive days Result: Caused a 100% reduction of the mean tumor volume within 4 weeks. Animal Model: 8-12 weeks, C57BL/6N mice (CML-like disease mouse model)[1] Dosage: 50 mg/kg Administration: P.o.; once daily for 20 days Result: Extended median survival significantly from 28 days to 39. |
| References |
| Molecular Formula | C29H27F3N6O |
|---|---|
| Molecular Weight | 532.56 |