Molecular Weight(MW): 442.94
LDN193189 HCl is the hydrochloride salt of LDN193189, which is a selective BMP signaling inhibitor, and inhibits the transcriptional activity of the BMP type I receptors ALK2 and ALK3 with IC50 of 5 nM and 30 nM in C2C12 cell lines, respectively, 200-fold selectivity for BMP versus TGF-β.
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LDN induces signifiant cell death. OVCA429 cells were treated with vehicle (DMSO) or experimental drugs for 6 hr to capture different stages of cell death. OVCA429 cell viability was assessed in response to drug treatment for 6 hr by staining with AO (green) and EB (orange). For clarity the different fluorescent channels to detect AO, EB, and the over-lapping images are shown for 10 mM LDN treatment.
Int J Cancer 2014 10.1002/ijc.29220. LDN-193189 HCl purchased from Selleck.
The density of muscle ?bers and myoseptum are partially rescued in morphants treated with LDN to decrease BMP signaling (D–F) .These were ?xed at 24 hpf and labeled with an antibody against Pax7, which strongly labels neural crest derived cells and also labels dermomyotome cells.
2014 378:107-121. LDN-193189 HCl purchased from Selleck.
Purity & Quality Control
Choose Selective TGF-beta/Smad Inhibitors
|Description||LDN193189 HCl is the hydrochloride salt of LDN193189, which is a selective BMP signaling inhibitor, and inhibits the transcriptional activity of the BMP type I receptors ALK2 and ALK3 with IC50 of 5 nM and 30 nM in C2C12 cell lines, respectively, 200-fold selectivity for BMP versus TGF-β.|
|Features||Selective BMP type I receptor inhibitor.|
LDN193189 potently inhibits BMP4-mediated Smad1, Smad5 and Smad8 activation with IC50 of 5 nM, and efficiently inhibits transcriptional activity of the BMP type I receptors ALK2 and ALK3 with IC50 of 5 nM and 30 nM, respectively. Furthermore, LDN193189 also shows the inhibitory effect on the transcriptional activity induced by either constitutively active ALK2R206H or ALK2Q207D mutant proteins.  A recent study shows that LDN-193189 blocks the production of reactive oxygen species induced by oxidized LDL during atherogenesis in human aortic endothelial cells. 
|In vivo||In conditional caALK2-transgenic mice with Ad.Cre on on postnatal day 7 (P7), LDN-193189 (3 mg/kg i.p) leads to mild calcifications surrounding the left tibia and fibula first visible at P13, and prevents radiographic lesions at P15 without causing weight loss or growth retardation, spontaneous fractures, decreased bone density or behavioral abnormalities.  LDN193189 dorsalizes zebrafish embryos by inhibiting signaling pathways induced by bone morphogenetic protein (BMP)6 without effect on vascular development.  In PCa-118b tumor-bearing mice, LDN-193189 treatment attenuates tumor growth and reduces bone formation in the tumors.  In LDL receptor-deficient (LDLR-/-) mice, LDN-193189 potently inhibits development of atheroma. Moreover, LDN-193189 also exhibits the inhibitory effects on associated vascular inflammation, osteogenic activity, and calcification. |
|In vitro||Water||52 mg/mL (117.39 mM)|
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