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Kobe0065

  Cat. No.:  DC7443   Featured
Chemical Structure
436133-68-5
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More than 5000 active chemicals with high quality for research!
Field of application
Kobe0065 is a novel and effective small-molecule compound inhibiting Ras–Raf interaction by SBDD; exhibits potent activity to competitively inhibit the binding of H-Ras·GTP to c-Raf-1 RBD with a Ki value of 46 ± 13 μM.
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 436133-68-5
Chemical Name: N-(3-Chloro-4-methylphenyl)-2-[2,6-dinitro-4-(trifluoromethyl)phenyl]-hydrazinecarbothioamide
Synonyms: N-(3-Chloro-4-methylphenyl)-2-[2,6-dinitro-4-(trifluoromethyl)phenyl]-hydrazinecarbothioamide;Kobe 0065;N-(3-CHLORO-4-METHYLPHENYL)-2-(2,6-DINITRO-4-(TRIFLUOROMETHYL)PHENYL)HYDRAZINECARBOTHIOAMIDE;N-(3-Chloro-4-methylphenyl)-2-[2,6-dinitro-4-(trifluoromethyl)phe nyl]hydrazinecarbothioamide;Kobe-0065;Kobe0065;C15H11ClF3N5O4S;N-(3-Chloro-4-methylphenyl)-2-[2,6-dinitro-4-(trifluoromethyl)phenyl]hydrazinecarbothioamide;SYN5190;AOB4259;BCP28010;s8303;3766AH;AK175816;CID 3827663
SMILES: ClC1C([H])=C(C([H])=C([H])C=1C([H])([H])[H])N([H])C(N([H])N([H])C1C(=C([H])C(C(F)(F)F)=C([H])C=1[N+](=O)[O-])[N+](=O)[O-])=S
Formula: C15H11ClF3N5O4S
M.Wt: 449.7922
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Kobe0065 is a novel and effective inhibitor of Ras-Raf interaction, competitively inhibiting the binding of H-Ras·GTP to c-Raf-1 RBD with a Ki value of 46±13 μM.
In Vivo: Kobe0065 and Kobe2602 exhibit antitumor activity on a xenograft of human colon carcinoma SW480 cells carrying the K-ras(G12V) gene by oral administration[1].
In Vitro: Kobe0065-family compounds bind to Ras•GTP and exhibit antiproliferative activity toward cancer cells carrying the activated ras oncogenes. The compounds efficiently inhibit the interaction of Ras•GTP with their multiple effectors including Raf, PI3K, and RalGDS and a regulator/effector Sos and show rather broad binding specificity toward various Ras family small GTPases, which may account for their higher potency at the cellular level compared with that of the in vitro binding inhibition[1]. The phosphorylation of downstream kinases MEK and ERK is effectively attenuated by 20 μM Kobe0065 and Kobe2602 in NIH3T3 cells transiently expressing H-RasG12V[2].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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