For research use only. Not for therapeutic Use.
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. Vamotinib inhibits ABL series kinases with IC50s of 0.49 nM (ABL), 0.78 nM (ABLT315I), 9.5 nM (ABLE255K), 2.0 nM (ABLF317I), 7.4 nM (ABLG250E), 1.0 nM (ABLH396P), 2.8 nM (ABLM351T), 12 nM (ABLQ252H), and 4.1 nM (ABLY253F), respectively[1][2]. Vamotinib is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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].
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].
| Catalog Number | I043359 |
| CAS Number | 1416241-23-0 |
| Synonyms | 4-methyl-N-[4-[(4-methylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl]-3-[2-([1,2,4]triazolo[4,3-a]pyridin-3-yl)ethynyl]benzamide |
| Molecular Formula | C29H27F3N6O |
| Purity | ≥95% |
| InChI | InChI=1S/C29H27F3N6O/c1-20-6-7-22(17-21(20)9-11-27-35-34-26-5-3-4-12-38(26)27)28(39)33-24-10-8-23(25(18-24)29(30,31)32)19-37-15-13-36(2)14-16-37/h3-8,10,12,17-18H,13-16,19H2,1-2H3,(H,33,39) |
| InChIKey | SLIVDYMORZGPLW-UHFFFAOYSA-N |
| SMILES | CC1=C(C=C(C=C1)C(=O)NC2=CC(=C(C=C2)CN3CCN(CC3)C)C(F)(F)F)C#CC4=NN=C5N4C=CC=C5 |
| Reference | [1]. Mian AA, et al. PF-114, a potent and selective inhibitor of native and mutated BCR/ABL is active against Philadelphia chromosome-positive (Ph+) leukemias harboring the T315I mutation. Leukemia. 2015 May;29(5):1104-14. [2]. Mian AA,et al. PF-114, a potent and selective inhibitor of native and mutated BCR/ABL is active against Philadelphia chromosome-positive (Ph+) leukemias harboring the T315I mutation. Leukemia. 2015 May;29(5):1104-14. [3]. Ivanova ES, et al. PF‑114, a novel selective inhibitor of BCR‑ABL tyrosine kinase, is a potent inducer of apoptosis in chronic myelogenous leukemia cells. Int J Oncol. 2019 Jul;55(1):289-297. |
