251356-45-3
251356-45-3
Chemical Structure
SU16f
- CAS No.: 251356-45-3
- Formula:C24H22N2O3
- Molecular Weight:386.44
IUPAC Name: (Z)-3-(2,4-dimethyl-5-((2-oxo-6-phenylindolin-3-ylidene)methyl)-1H-pyrrol-3-yl)propanoic acid
InChIKey: APYYTEJNOZQZNA-MOSHPQCFSA-N
SMILES: O=C(O)CCC1=C(C)NC(/C=C2C(NC3=C\2C=CC(C4=CC=CC=C4)=C3)=O)=C1C
Biological Activity: SU16f is a potent and selective PDGFRβ inhibitor with IC50s of 10 nM, 140 nM, 2.29 μM for PDGFRβ, VEGF-R2, FGF-R1, respectively[1]. Neutralization of PDGFRβ receptor by SU16f blocks the promoting role of GC-MSCs (gastric cancer-derived mesenchymal stem cells) conditioned medium in gastric cancer cell proliferation and migration[2].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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SU16f | 99.36% | SU16f is a potent and selective PDGFRβ inhibitor with IC50s of 10 nM, 140 nM, 2.29 μM for PDGFRβ, VEGF-R2, FGF-R1, respectively. Neutralization of PDGFRβ receptor by SU16f blocks the promoting role of GC-MSCs (gastric cancer-derived mesenchymal stem cells) conditioned medium in gastric cancer cell proliferation and migration. | ||||||||||||||||||||
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SU16f (Standard) | ≥98% | SU16f (Standard) is the analytical standard of SU16f (HY-108628). This product is intended for research and analytical applications. SU16f is a potent and selective PDGFRβ inhibitor with IC50s of 10 nM, 140 nM, 2.29 μM for PDGFRβ, VEGF-R2, FGF-R1, respectively. Neutralization of PDGFRβ receptor by SU16f blocks the promoting role of GC-MSCs (gastric cancer-derived mesenchymal stem cells) conditioned medium in gastric cancer cell proliferation and migration. | ||||||||||||||||||||
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References
- [1]. Sun L, et al. Design, synthesis, and evaluations of substituted 3-[(3- or 4-carboxyethylpyrrol-2-yl)methylidenyl]indolin-2-ones as inhibitors of VEGF, FGF, and PDGF receptor tyrosine kinases. J Med Chem. 1999 Dec 16;42(25):5120-30. [Content Brief]
- [2]. Huang F, et al. Gastric cancer-derived MSC-secreted PDGF-DD promotes gastric cancer progression. J Cancer Res Clin Oncol. 2014 Nov;140(11):1835-48. [Content Brief]
