SNX2-1-165; BCD-115 MedChemExpress (MCE)

Product Name	Senexin B
Synonyms	Senexin B SNX2-1-165 Senexin B (SNX2-1-165) 4-(2-(6-(4-methylpiperazine-1-carbonyl)naphthalen-2-yl)ethylamino)quinazoline-6-carbonitrile 6-Quinazolinecarbonitrile, 4-[[2-[6-[(4-methyl-1-piperazinyl)carbonyl]-2-naphthalenyl]ethyl]amino]-
CAS	1449228-40-3
EINECS
Chemical Formula	C27H26N6O
Molecular Weight	450.53
inchi
Package	1 mg;5 mg;10 mg
Price	Email to quote
Descriptions	Senexin B Senexin B MedChemExpress (MCE) HY-101800 1449228-40-3 SNX2-1-165 Descriptions Senexin B Senexin B MedChemExpress (MCE) HY-101800 1449228-40-3 SNX2-1-165 BCD-115 99.72% Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Room temperature in continental US may vary elsewhere. Senexin B (SNX2-1-165 BCD-115) is a potent, highly water-soluble and bioavailable CDK8/19 inhibitor, with Kds of 140 nM for CDK8 and 80 nM for CDK19. Senexin B inhibits CDK8/19 in low nanomolar range[1]. Senexin B is a newly optimized derivative of Senexin A. It has the same high selectivity for CDK8/19 and is more potent than Senexin A. Senexin B strongly reduces the emergence of estrogen independent cells. Senexin B shows synergy with fulvestrant in MCF7, T47D-ER/Luc and BT474[2]. Pretreatment of tumor-free mice with Senexin B significantly inhibits the growth of triple-negative breast cancer (TNBC) cells inoculated into mice subsequently to Senexin B administration, indicating a general chemopreventive effect on the normal tissue "soil" . Senexin B potentiates the tumor-suppressive effect of doxorubicin on established TNBC xenografts this effect is associated with the suppression of NFκB-mediated transcriptional induction of tumor-promoting cytokines. Senexin B inhibits invasive growth into the muscle layer in an orthotopic xenograft model of MDA-MB-468 TNBC cells. In a spleen-to-liver colon cancer metastasis model of syngeneic mouse CT26 tumors, Senexin B treatment of mice have the same effect as CDK8 knockdown in tumor cells: suppression of metastatic growth in the liver without a significant effect on primary tumor growth in the spleen[1]. Senexin B suppresses tumor growth and augmentes the effects of fulvestrant in ER-positive breast cancer xenografts[2]. Mice: Once tumors reach 100-200 mm3 volume, 4 groups of mice are treated with vehicle, Senexin B dimaleate (100 mg/kg twice daily, oral gavage in 6.25% 2-Hydroxypropyl-β-cyclodextrin, 1% Dextrose buffer) alone or in combination with fulvestrant (5 mg/mouse s.c once/week). Tumor volumes are measured twice weekly with calipers and volumes are calculated. After 40 days mice are euthanized, tumors are excised and weighed[2]. CDK19 80 nM (Kd) CDK8 140 nM (Kd) \| \| \| \| \| \| \| \| \| \| [1]. Porter D, et al. Abstract PR08: Targeting tumor microenvironment with selective small-molecule inhibitors of CDK8/19. Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment 2014 Feb 26-Mar 1 San Diego, CA. Philadelphia (PA): AACR Cancer Res 2015 75(1 Suppl):Abstract nr PR08. doi:10.1158/1538-7445.CHTME14-PR08 [2]. McDermott MS, et al. Inhibition of CDK8 mediator kinase suppresses estrogen dependent transcription and the growth of estrogen receptor positive breast cancer. Oncotarget. 2017 Feb 21 8(8):12558-12575. [Content Brief] [3]. CDK8-CDK19 selective inhibitors and their use in anti-metastatic and chemopreventative methods for cancer. US 9321737 B2
Last Update	2025-04-01 14:45:47

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