[CAS NO. 1415560-69-8]  Crizotinib hydrochloride

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PRODUCTS SPECIFICATIONS [1415560-69-8]

Catalog
SLK-S5190
Brand
Selleck
CAS
1415560-69-8

DESCRIPTION [1415560-69-8]

Overview

MDL-
Molecular Weight486.8
Molecular FormulaC21H23Cl3FN5O
SMILESO([C@H](C)C1=C(Cl)C(F)=CC=C1Cl)C2=CC(C3=CN(N=C3)C4CCNCC4)=CN=C2N.Cl

For research use only.

Storage

3 years,-20°C,powder
1 years,-80°C,in solvent

Shipping

Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

1 mg5 mg10 mg
1 mM2.0542 mL10.2712 mL20.5423 mL
5 mM0.4108 mL2.0542 mL4.1085 mL
10 mM0.2054 mL1.0271 mL2.0542 mL
50 mM0.0411 mL0.2054 mL0.4108 mL

Description

Crizotinib (PF-02341066) hydrochloride (Xalkori) inhibits tyrosine phosphorylation of and nucleophosmin (NPM)- with IC50 of of 11 nM and 24 nM in cell-based assays, respectively. Crizotinib hydrochloride is also a potent inhibitor with Ki less than 0.025 nM. Crizotinib induces through inhibition of the STAT3 pathway in multiple lung cancer cell lines.

Targets

ROS1 [2]
(Cell-free assay)
c-Met [1]
(Cell-based assay)
NPM-ALK [2]
(Cell-based assay)
<0.025 nM(Ki)11 nM24 nM

In vitro

PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively. PF-2341066 is >1,000-fold selective for the VEGFR2 and PDGFRβ RTKs, >250-fold selective for IRK and Lck, and ∼40- to 60-fold selective for Tie2, TrkA, and TrkB, all compared with c-Met. PF-2341066 is 20- to 30-fold selective for RON and Axl RTKs. In contrast, PF-2341066 shows a near-equivalent IC50 of 24 nM against the nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) oncogenic fusion variant of the ALK RTK expressed by the KARPAS299 human anaplastic large cell lymphoma (ALCL) cell line. PF-2341066 inhibits c-Met–dependent neoplastic phenotypes of cancer cells and angiogenic phenotypes of endothelial cells. PF-2341066 suppresses human GTL-16 gastric carcinoma cell growth with IC50 of 9.7 nM. PF-2341066 induces apoptosis in GTL-16 cells with IC50 of 8.4 nM. PF-2341066 inhibits HGF-stimulated human NCI-H441 lung carcinoma cell migration and invasion with IC50 of 11 nM and 6.1 nM, respectively. PF-2341066 inhibits MDCK cell scattering with IC50 of 16 nM. PF-2341066 prevents HGF-stimulated c-Met phosphorylation, cell survival, and Matrigel invasion with IC50 of 11 nM, 14 nM and 35 nM, respectively. In addition, PF-2341066 prevents serum-stimulated HMVEC branching tubulogenesis (formation of vascular tubes) in fibrin gels.


Synonyms

2-Pyridinamine, 3-[(1R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(4-piperidinyl)-1H-pyrazol-4-yl]-, hydrochloride (1:1)