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SML1422

Sigma-Aldrich

CCG-203971

≥98% (HPLC)

Synonym(s):

N-(4-Chlorophenyl)-1-[3-(2-furanyl)benzoyl]-3-piperidinecarboxamide

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About This Item

Empirical Formula (Hill Notation):
C23H21ClN2O3
CAS Number:
1443437-74-8
Molecular Weight:
408.88
MDL number:
MFCD28166491
UNSPSC Code:
12352200
PubChem Substance ID:
329825865
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

white to beige

storage temp.

2-8°C

SMILES string

ClC(C=C1)=CC=C1NC(C(C2)CCCN2C(C3=CC(C4=CC=CO4)=CC=C3)=O)=O

InChI

1S/C23H21ClN2O3/c24-19-8-10-20(11-9-19)25-22(27)18-6-2-12-26(15-18)23(28)17-5-1-4-16(14-17)21-7-3-13-29-21/h1,3-5,7-11,13-14,18H,2,6,12,15H2,(H,25,27)

InChI key

HERLZBNILRVHQN-UHFFFAOYSA-N

Biochem/physiol Actions

CCG-203971 is an inhibitor of the Rho/MKL1/SRF transcriptional pathway, which has been shown to play a role in metastasis of melanoma and breast cancer and clinically associated with castration-resistant prostate cancer. CCG-203971 is a second-generation analog of CCG-1423 (SML0987) with an IC50 of 4.2 μM vs 1 μM for CCG-1423, but less cytotoxicity. In mouse studies, CCG-203971 inhibited invasion of PC-3 prostate cancer cells and was well tolerated up to doses of 100 mg/kg IP over 5 days.

The Rho/MRTF/SRF pathway has also been shown to be involved in multiple types of solid organ fibrosis. CCG-203971 repressed both matrix-stiffness and TGF-β-mediated fibrogenesis in human colonic myofibroblasts and showed antifibrotic activity in a murine model of skin injury and in pulmonary fibrosis lung fibroblasts.

pictograms

Exclamation mark
GHS07

signalword

Warning

hcodes

H302

Hazard Classifications

Acute Tox. 4 Oral

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Many tissues harbor quiescent stem cells that are activated upon injury, subsequently proliferating and differentiating to repair tissue damage. Mechanisms by which stem cells sense injury and transition from quiescence to activation, however, remain largely unknown. Resident skeletal muscle stem

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