Golvatinib
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MedKoo CAT#: 201072

CAS#: 928037-13-2

Description: Golvatinib, also known as E7050, is an orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. c-Met/VEGFR kinase inhibitor E7050 binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of various tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.


Price and Availability

Size
Price

10mg
USD 90
100mg
USD 450
1g
USD 2150
10g
USD 5950
Size
Price

25mg
USD 150
200mg
USD 650
2g
USD 3650
20g
Ask price
Size
Price

50mg
USD 250
500mg
USD 1250
5g
USD 4750

Golvatinib (or E7050), purity > 98%, is in stock. The same day shipping out after order is received.


Chemical Structure

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Theoretical Analysis

MedKoo Cat#: 201072
Name: Golvatinib
CAS#: 928037-13-2
Chemical Formula: C33H37F2N7O4
Exact Mass: 633.28751
Molecular Weight: 633.69
Elemental Analysis: C, 62.55; H, 5.89; F, 6.00; N, 15.47; O, 10.10


Synonym: E7050; E-7050; E 7050; Golvatinib.

IUPAC/Chemical Name: N-(2-fluoro-4-((2-(4-(4-methylpiperazin-1-yl)piperidine-1-carboxamido)pyridin-4-yl)oxy)phenyl)-N-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide

InChi Key: BWEYRDZIIMFBJR-UHFFFAOYSA-N

InChi Code: InChI=1S/C33H37F2N7O4/c1-39-16-18-40(19-17-39)23-9-14-41(15-10-23)32(45)38-29-21-26(8-13-37-29)46-25-6-7-28(27(35)20-25)42(24-4-2-22(34)3-5-24)31(44)33(11-12-33)30(36)43/h2-8,13,20-21,23H,9-12,14-19H2,1H3,(H2,36,43)(H,37,38,45)

SMILES Code: O=C(C1(C(N)=O)CC1)N(C2=CC=C(OC3=CC(NC(N4CCC(N5CCN(C)CC5)CC4)=O)=NC=C3)C=C2F)C6=CC=C(F)C=C6


Technical Data

Appearance:
white solid powder

Purity:
>98% (or refer to the Certificate of Analysis)

Certificate of Analysis:

Safety Data Sheet (MSDS):

Shipping Condition:
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition:
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility:
Soluble in DMSO, not in water

Shelf Life:
>2 years if stored properly

Drug Formulation:
This drug may be formulated in DMSO

Stock Solution Storage:
0 - 4 C for short term (days to weeks), or -20 C for long term (months).

Harmonized System Code:
293490


Additional Information

E7050 is the first kinase inhibitor with dual action against both c-Met and VEGFR-2. The dual inhibitory activity of E7050 against tumor growth and angiogenesis results in drastic tumor regression and disappearance and also prolongation of lifespan without adverse effects.  E7050 is currently under evaluation in a phase I clinical trial.    ( Cancer Sci . 2010 Jan;101(1):210-5. Epub 2009 Sep 2.).
E7050 is the first kinase inhibitor with dual action against both c-Met and VEGFR-2. The dual inhibitory activity of E7050 against tumor growth and angiogenesis results in drastic tumor regression and disappearance and also prolongation of lifespan without adverse effects.  E7050 is currently under evaluation in a phase I clinical trial.    (
).
    
  
E7050 circumvented resistance to all of the reversible, irreversible, and mutant-selective EGFR-TKIs induced by exogenous and/or endogenous HGF in EGFR mutant lung cancer cell lines, by blocking the Met/Gab1/PI3K/Akt pathway in vitro. E7050 also prevented the emergence of gefitinib-resistant HCC827 cells induced by continuous exposure to HGF. In the in vivo model, E7050 plus gefitinib resulted in marked regression of tumor growth associated with inhibition of Akt phosphorylation in cancer cells. CONCLUSIONS: A new Met kinase inhibitor, E7050, reverses the three HGF-induced mechanisms of gefitinib resistance, suggesting that E7050 may overcome HGF-induced resistance to gefitinib and next-generation EGFR-TKIs. (source: Clin Cancer Res. 2012 Mar 15;18(6):1663-71. Epub 2012 Feb 8.)
E7050 circumvented resistance to all of the reversible, irreversible, and mutant-selective EGFR-TKIs induced by exogenous and/or endogenous HGF in EGFR mutant lung cancer cell lines, by blocking the Met/Gab1/PI3K/Akt pathway in vitro. E7050 also prevented the emergence of gefitinib-resistant HCC827 cells induced by continuous exposure to HGF. In the in vivo model, E7050 plus gefitinib resulted in marked regression of tumor growth associated with inhibition of Akt phosphorylation in cancer cells. CONCLUSIONS: A new Met kinase inhibitor, E7050, reverses the three HGF-induced mechanisms of gefitinib resistance, suggesting that E7050 may overcome HGF-induced resistance to gefitinib and next-generation EGFR-TKIs. (source:
)


References

1: Nakagawa T, Takeuchi S, Yamada T, Nanjo S, Ishikawa D, Sano T, Kita K, Nakamura T, Matsumoto K, Suda K, Mitsudomi T, Sekido Y, Uenaka T, Yano S. Combined Therapy with Mutant-Selective EGFR Inhibitor and Met Kinase Inhibitor for Overcoming Erlotinib Resistance in EGFR-Mutant Lung Cancer. Mol Cancer Ther. 2012 Oct;11(10):2149-57. doi: 10.1158/1535-7163.MCT-12-0195. Epub 2012 Jul 25. PubMed PMID: 22844075.

2: Takeuchi S, Wang W, Li Q, Yamada T, Kita K, Donev IS, Nakamura T, Matsumoto K, Shimizu E, Nishioka Y, Sone S, Nakagawa T, Uenaka T, Yano S. Dual inhibition of Met kinase and angiogenesis to overcome HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer. Am J Pathol. 2012 Sep;181(3):1034-43. doi: 10.1016/j.ajpath.2012.05.023. Epub 2012 Jul 9. PubMed PMID: 22789825.

3: Wang W, Li Q, Takeuchi S, Yamada T, Koizumi H, Nakamura T, Matsumoto K, Mukaida N, Nishioka Y, Sone S, Nakagawa T, Uenaka T, Yano S. Met kinase inhibitor E7050 reverses three different mechanisms of hepatocyte growth factor-induced tyrosine kinase inhibitor resistance in EGFR mutant lung cancer. Clin Cancer Res. 2012 Mar 15;18(6):1663-71. Epub 2012 Feb 8. PubMed PMID: 22317763.

4: Green DR. 'Tit-for-tat' in cell biology. Nat Rev Mol Cell Biol. 2011 Feb;12(2):73. PubMed PMID: 21252991.

5: Nakagawa T, Tohyama O, Yamaguchi A, Matsushima T, Takahashi K, Funasaka S, Shirotori S, Asada M, Obaishi H. E7050: a dual c-Met and VEGFR-2 tyrosine kinase inhibitor promotes tumor regression and prolongs survival in mouse xenograft models. Cancer Sci. 2010 Jan;101(1):210-5. Epub 2009 Sep 2. PubMed PMID: 19832844.