Chemical Name |
DMH-1 |
CAS Number |
1206711-16-1 |
MDL Number |
MFCD18384963 |
Molecular Formula |
C24H20N4O |
Molecular Weight |
380.44 |
Introduction of 1206711-16-1 :
DMH-1 is a potent and selective BMP inhibitor with IC50s of 27/107.9/<5/47.6 nM for ALK1/ALK2/ALK3/ALK6, respectively. IC50 & Target: IC50: 27 nM (ALK1), 107.9 nM (ALK2), <5 nM (ALK3), 47.6 nM (ALK6)[1] In Vitro: DMH-1 (0.5 μM) induces regulation of OCT4, Nanog, and PAX6 protein expression. DMH-1 significantly reduces the percentage of cells expressing the pluripotency marker proteins OCT4 and Nanog in both SM3 and CA6 cells. PAX6 expression is significantly up-regulated by day 5 and day 7 in CA6 and SM3 cells, respectively. DMH-1 induces regulation of pluripotency and neural precursor marker mRNAs. PAX6 can regulate the expression of SOX1 independently by manipulating the DMH-1 concentration during the neural induction of hiPSCs[2]. DMH-1 (5 μM and 10 μM) inhibits CDDP-induced autophagy in HeLa cells and enhances the ability of CDDP to reduce HeLa cell viability, inhibits tamoxifen-induced autophagy in MCF-7 cells and enhances the ability of tamoxifen to reduce MCF-7 cell viability, inhibits 5-FU-induced autophagy in both MCF-7 and HeLa cells but does not affect the inhibitory effects of 5-FU on MCF-7 and HeLa cell viability. DMH-1 enhances the apoptotic induction effects of CDDP on HeLa cells after 24 h treatment. DMH-1 inhibits HeLa and MCF-7 cell proliferation[3]. DMH-1 (20 μM) reduces the canonical phosphorylation of Smads 1,5 and 9. DMH-1 in combination with Cisplatin significantly decreases Ki-67 positive staining in the OVCAR8 cells. DMH-1 (20 µM) upregulates JAG1, reduces CYP1B1 and increases HAPLN1 expression in both OVCAR8 and NCI-RES cells[4]. In Vivo: DMH1 (5 mg/kg, i.p.) treatment significantly reduces the tumor growth in human lung cancer xenograft model[5].
Purity |
NLT 98% |
Storage |
at 20ºC 2 years |
*The above information is for reference only.