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執大象，天下往，往而無害，安平泰
WEB: www.eosmedchem.com
EMAIL: info@eosmedchem.com; eosmedchem@gmail.com; eosmedchem@qq.com
TEL: 0086-531-69905422
GMP PLANT: No. 37, Yulong Road, Qufu City, Shandong Province.
Description: PFK-158, also known as ACT-PFK-158, is an inhibitor of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFK-2/FBPase) isoform 3 (PFKFB3) with potential antineoplastic activity. Upon administration, PFKFB3 inhibitor PFK-158 binds to and inhibits the activity of PFKFB3, which leads to the inhibition of both the glycolytic pathway in and glucose uptake by cancer cells. This prevents the production of macromolecules and energy that causes the enhanced cellular proliferation in cancer cells as compared to that of normal, healthy cells. Depriving cancer cells of nutrients and energy leads to the inhibition of cancer cell growth.
Name: PFK-158
CAS#: 1462249-75-7
Chemical Formula: C18H11F3N2O
Exact Mass: 328.08235
Molecular Weight: 328.29
Elemental Analysis: C, 65.85; H, 3.38; F, 17.36; N, 8.53; O, 4.87
Synonym: PFK158; PFK 158; PFK158; ACTPEK158.
IUPAC/Chemical Name: (E)-1-(pyridin-4-yl)-3-(7-(trifluoromethyl)quinolin-2-yl)prop-2-en-1-one
InChi Key: IAJOMYABKVAZCN-AATRIKPKSA-N
InChi Code: InChI=1S/C18H11F3N2O/c19-18(20,21)14-3-1-12-2-4-15(23-16(12)11-14)5-6-17(24)13-7-9-22-10-8-13/h1-11H/b6-5+
SMILES Code: O=C(C1=CC=NC=C1)/C=C/C2=NC3=CC(C(F)(F)F)=CC=C3C=C2
Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility: Soluble in DMSO, not in water
Shelf Life: >2 years if stored properly
Drug Formulation: This drug may be formulated in DMSO
Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).
Harmonized System Code: 293490
ADDITIONAL INFORMATION
The PFKFB enzymes (PFKFB 1- 4) synthesize fructose-2,6-bisphosphate (F2,6BP) which activates 6-phosphofructo-l- kinase (PFK-1), an essential control point in the glycolytic pathway. Neoplastic cells preferentially utilize glycolysis to satisfy their increased needs for energy and biosynthetic precursors. Malignant tumor cells have glycolytic rates that are up to 200 times higher than those of their normal tissues of origin. One cancer attack strategy has been to treat cancer by starving cancerous cells in various ways. Reducing or blocking the enhanced glycolytic flux mechanism present in cancer cells has stimulated recent interest. Despite greater understanding and pharmaceutical advances in the diagnosis and treatment of cancer, it is still estimated that nearly 13% of all human deaths last year were due to cancer. Thus, there remains a need for safe and effective anti-cancer therapeutics, particularly those which target neoplastic cells via mechanisms such as glycolytic flux, which are over-expressed in cancer cells. (http://www.google.com/patents/WO2013148228A1?cl=en)
