NSC12

Catalog No.S7940 Synonyms: NSC 172285

NSC12 Chemical Structure

Molecular Weight(MW): 484.52

NSC12 is an orally available pan-FGF trap able to inhibit FGF2/FGFR interaction and endowed with promising antitumor activity.

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Biological Activity

Description NSC12 is an orally available pan-FGF trap able to inhibit FGF2/FGFR interaction and endowed with promising antitumor activity.
Targets
FGF3 [1]
(Cell-free assay)
FGF8b [1]
(Cell-free assay)
FGF22 [1]
(Cell-free assay)
FGF20 [1]
(Cell-free assay)
FGF2 [1]
(Cell-free assay)
15.9 μM(Kd) 18.9 μM(Kd) 26.8 μM(Kd) 29.4 μM(Kd) 51 μM(Kd)
In vitro

NSC12 inhibits FGF-dependent tumor growth, angiogenesis, and metastases. NSC12 does not affect FGF2/heparin interaction, whereas it inhibits the binding of FGF2 to the immobilized receptor (ID50 ∼30 μM). NSC12 interferes with FGF2/FGFR1 interaction without affecting the ability of the growth factor to interact with heparin or HSPGs. NSC12 also binds immobilized FGF3, FGF4, FGF6, FGF8, FGF16, FGF18, FGF20, and FGF22 with Kd values ranging between ∼16 and ∼120 μM. NSC12 may act as a multi-FGF trap by interacting with all members of the canonical FGF subfamilies. NSC12 hampers FGF23-mediated FGFR1 activation in Klotho-expressing Chinese hamster ovary (CHO) cells. Treatment with NSC12 causes the reduction of the S phase of the cell cycle in all tumor cell lines but LLC cells, in which an accumulation in the S phase is observed. NSC12 inhibits FGFR1, FGFR2, FGFR3, and FGFR4 phosphorylation in CHO cell transfectants. NSC12 inhibits the proliferation of various FGF-dependent murine and human cancer cell lines with no inhibitory effect on HCC827 cancer cells that harbor a tumor-driving mutation of the EGFR TK domain and on FGF-independent cancer cell lines[1].

In vivo Parenteral and oral delivery of NSC12 inhibits FGFR activation, tumor growth, angiogenesis, and metastasis in FGF-dependent murine and human tumor models. NSC12 causes a significant decrease of tumor weight, tumor cell FGFR1 phosphorylation and proliferation, and tumor CD31+ neovascularization at all the doses tested in the animal models[1].

Protocol

Cell Research:[1]
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  • Cell lines: KATO Ⅲ cells
  • Concentrations: 1.0 or 3.0 μM
  • Incubation Time: 72 h
  • Method: KATO Ⅲ cells are plated at 104 cells/well in 96 well-plates in RPMI medium plus 1% FBS. After 24 hr cells are treated with different FGFs (30 ng/ml) in the absence or presence of an optimal dose of NSC12 (1.0 or 3.0 μM) or NSC21. After 72 hr the MTT assay is performed according to manufacturer’s instructions. The optical density (OD) is determined using a plate reader at a test wavelength of 595 nm and a reference wavelength of 630 nm.
    (Only for Reference)
Animal Research:[1]
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  • Animal Models: C57BL/6 mice
  • Formulation: DMSO
  • Dosages: from 2.5 to 10 mg/kg
  • Administration: i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 96 mg/mL (198.13 mM)
Ethanol 63 mg/mL (130.02 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 484.52
Formula

C24H34F6O3

CAS No. 102586-30-1
Storage powder
in solvent
Synonyms NSC 172285

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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FGFR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID