Alvocidib - CAS 146426-40-6
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
Alvocidib
Catalog Number:
B0084-059050
Synonyms:
Flavopiridol; HMR 1275.
CAS Number:
146426-40-6
Description:
Alvocidib is a synthetic N-methylpiperidinyl chlorophenyl flavone compound. As an inhibitor of cyclin-dependent kinase, alvocidib induces cell cycle arrest by preventing phosphorylation of cyclin-dependent kinases (CDKs) and by down-regulating cyclin D1 and D3 expression, resulting in G1 cell cycle arrest and apoptosis.
COA:
Inquire
MSDS:
Inquire
Targets:
CDK
Current Developer:
Sanofi-Aventis Inc.
Chemical Structure
CAS 146426-40-6 Alvocidib

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Reference Reading


1. Flavonoids from Achyrocline satureioides: promising biomolecules for anticancer therapy
Juliana Poglia Carini*, F´ abio Klamt, Valquiria Linck Bassani. RSC Adv.,2014, 4,3131–3144
Flavopiridol is another semisynthetic avonoid with potential anticancer properties. The compound is a flavone derived from rohitukine, a natural anticancer agent isolated from an Indian tree. Due to its interesting biological properties both in vitro and in vivo, as cell cycle arrest in G1 and G2 phases, cytotoxicity against the majority of tumor cell lines in the nanomolar range, suppression of the tumor growth in animals and synergistic activity with most anticancer drugs and radiation, flavopiridol was the first cyclin-dependent kinase (CDK) inhibitor to be tested in human clinical trials. However, the molecule in Phase II clinical trials was ineffective against cancer and presented high toxicity to patients. Nevertheless, currently 60 anticancer clinical trials can be found with flavopiridol, alone or combined with other drugs, whereby 6 of them have shown to be active in the recruiting phase.
2. Mutual interactions between flavonoids and enzymatic and transporter elements responsible for flavonoid disposition via phase II metabolic pathways
Wen Jiang, Ming Hua. RSC Adv., 2012, 2, 7948–7963
Early investigation showed that genistein inhibited the efflux of daunorubicin from small-cell lung cancer GL4/ADR cells, in which MRP was overexpressed, in a competitive manner. The same result of inhibition of daunorubicin by genistein competitively was also observed in plasma membrane vesicles from marine MRP-transfected NIH3T3 cells. Follow-up study confirmed that genistein but not genistin, together with kaempferol and flavopiridol (synthetic flavonoid derivative) could affect MRP-mediated transport of anticancer drugs by a direct interaction with MRP. Moreover, chrysin was reported to inhibit the accumulation of the MRP2 substrate CMFDA in Caco-2 cells in a dose-dependent manner. The maximal accumulation, which could also be achieved by specific MRP inhibitor-MK571, was observed in the presence of 250 mM chrysin. Interestingly, chrysin was also found to increase the expression of MRP2 5 fold in Caco-2 cells after long-term treatment. Over a time period of 48 h, the inhibition of transporter function overtook the enhanced expression of MRP2 by chrysin, resulting in an increased accumulation of topotecan. Therefore, chrysin seemed to play a dual role in regulating MRP2 in Caco-2 cells.