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Key Documents

SML0965

Sigma-Aldrich

LDN-212854

≥98% (HPLC)

Synonyme(s) :

5-[6-[4-(1-Piperazinyl)phenyl]pyrazolo[1,5-a]pyrimidin-3-yl]-quinoline

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About This Item

Formule empirique (notation de Hill):
C25H22N6
Numéro CAS:
1432597-26-6
Poids moléculaire :
406.48
Code UNSPSC :
51111800
Nomenclature NACRES :
NA.77

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 1 mg/mL, clear (warmed)

Température de stockage

2-8°C

InChI

1S/C25H22N6/c1-3-21(22-4-2-10-27-24(22)5-1)23-16-29-31-17-19(15-28-25(23)31)18-6-8-20(9-7-18)30-13-11-26-12-14-30/h1-10,15-17,26H,11-14H2

Clé InChI

BBDGBGOVJPEFBT-UHFFFAOYSA-N

Actions biochimiques/physiologiques

LDN-212854 is a selective and potent inhibitor of the bone morphogenetic protein (BMP) type I receptor kinases with over 5,000-fold selectivity for BMP versus the closely related TGF-β and activin type I receptors. LDN-212854 has some selectivity for ALK2 with an IC50 of 1.3 nM in preference to other BMP type I receptors, ALK1 (IC50=2.4 nM) and ALK3 (IC50=85.8 nM). LDN-212854 shows better selectivity than LDN193189 in cell-based assays of BMP signaling. LDN-212854 inhibited BMP6-induced osteogenic differentiation, which functions primarily via ALK2, more potently than BMP4, which functions primarily with ALK3 (IC50s of 10 nM versus 40.5 nM), whereas LDN-193189 inhibited both equally. The only off target effects found against a panel of 198 kinases were for RIPK2, ABL1, and PDGFR-β with IC50 values < 100 nM.
LDN-212854 is also known as 5-[6-[4-(1-Piperazinyl)phenyl]pyrazolo[1,5-a]pyrimidin-3-yl]-quinoline. LDN-212854 prevents heterotopic ossification in an inducible mutant ALK2 (activin receptor-like kinase 2).

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

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The Inhibitor Index: A Desk Reference on Enzyme Inhibitors, Receptor Antagonists, Drugs, Toxins, Poisons, Biologics, and Therapeutic Leads (2017)
Huili Zhang et al.
American journal of physiology. Lung cellular and molecular physiology, 313(3), L615-L627 (2017-06-24)
The intracellular signaling mechanisms through which TGF-β regulates pulmonary development are incompletely understood. Canonical TGF-β signaling involves Smad2/3 phosphorylation, Smad2/3·Smad4 complex formation and nuclear localization, and gene regulation. Here, we show that physiologically relevant TGF-β1 levels also stimulate Smad1/5 phosphorylation
Hongen Yin et al.
Scientific reports, 10(1), 2967-2967 (2020-02-23)
Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease, with only palliative treatments available. Recent work has suggested that increased bone morphogenetic protein 6 (BMP6) expression could alter cell signaling in the salivary gland (SG) and result in the associated

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