NSC12

Catalog No.S7940 Batch:S794001

Technical Data

Formula

C₂₄H₃₄F₆O₃

Molecular Weight

484.52

CAS No.

102586-30-1

Solubility (25°C)*

In vitro

Ethanol

63 mg/mL (130.02 mM)

DMSO

10.3 mg/mL (21.25 mM)

Water

Insoluble

In vivo (Add solvents to the product individually and in order)

Clear solution

5%DMSO 1 40%PEG300 2 5%Tween80 3 50%ddH2O

0.5mg/ml

Taking the 1 mL working solution as an example, add 50 μL of 10 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results.

* <1 mg/ml means slightly soluble or 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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description

NSC12 (NSC 172285) 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/FGFR ^[1] (Cell-free assay)	View More
15.9 μM(Kd)	18.9 μM(Kd)	26.8 μM(Kd)	29.4 μM(Kd)	30 μM	View More

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 (from reference)

Cell Assay:^{^[1]}	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.
Animal Study:^{^[1]}	Animal Models C57BL/6 mice Dosages from 2.5 to 10 mg/kg Administration i.p.

Cell Assay:^{^[1]}

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.

Animal Study:^{^[1]}

Animal Models
C57BL/6 mice
Dosages
from 2.5 to 10 mg/kg
Administration
i.p.

References

[1] Ronca R, et al. Cancer Cell. 2015, 28(2):225-39.

Selleck's NSC12 has been cited by 2 publications

VC-resist glioblastoma cell state: vessel co-option as a key driver of chemoradiation resistance [ Nat Commun, 2024, 15(1):3602]	PubMed: 38684700
MiR-148b-3p inhibits renal carcinoma cell growth and pro-angiogenic phenotype of endothelial cell potentially by modulating FGF2. [Zhang H, et al. Biomed Pharmacother, 2018, 107:359-367]	PubMed: 30099339

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.