STATIL

Statil is an aldose reductase inhibitor that blocks the conversion of glucose to sorbitol. It demonstrates selectivity for aldose reductase 2 over aldose reductase 1 with K_i values of 7.7 nM and 60 μM, respectively. Statil has been shown to prevent diabetes-induced alterations of the cardiovascular system in 14-day streptozotocin-diabetic rats. Aldose reductase inhibition by statil has also been used to impair the synthesis of prostaglandin F_2α by human cultured preadipocytes.

Inhibitor (aldose reductase).

Statil is a knon aldose reductase inhibitor which blocks the conversion of glucose to sorbitol. In addition it suppresses cell cancer growth

ChEBI: 2-[3-[(4-bromo-2-fluorophenyl)methyl]-4-oxo-1-phthalazinyl]acetic acid is a member of phthalazines.

Potent aldose reductase inhibitor.

[1] WALTER H.J. WARD . Ponalrestat: A potent and specific inhibitor of aldose reductase[J]. Biochemical pharmacology, 1990, 39 2: Pages 337-346. DOI: 10.1016/0006-2952(90)90033-h
[2] DONNA J. OTTER  Russell C W. The effects of aldose reductase inhibition with ponalrestat on changes in vascular function in streptozotocin diabetic rats[J]. British Journal of Pharmacology, 1994, 113 2: 576-580. DOI: 10.1111/j.1476-5381.1994.tb17028.x
[3] ANDRéANNE MICHAUD. Prostaglandin (PG) F2 alpha synthesis in human subcutaneous and omental adipose tissue: modulation by inflammatory cytokines and role of the human aldose reductase AKR1B1.[J]. PLoS ONE, 2014: e90861. DOI: 10.1371/journal.pone.0090861