Disease relevance of HALOFENATE

• Our data establish halofenate as a novel SPPARgammaM with promising therapeutic utility with the potential for less weight gain [1].
• One such drug, halofenate, was indeed a safe and effective uricosuric (comparable to probenecid) when used to treat hyperuricemia/gout over the long term; it did result in a modest and variable fall in serum lipid concentrations [2].
• Clofibrate and its analogs (halofenate and beta-benzalbutyrate) produced significant hepatomegaly (mean responses of +18, +18 and +10%, respectively) whereas oxandrolone produced significant hepatic shrinkage (-10%)(P less than .05) [3].
• Twelve patients with Type IV hyperlipoproteinemia were treated with clofibrate and halofenate in a double blind, crossover trial for two years [4].
• Thus, halofenate is more potent than clofibrate in reducing the sensitivity of normal platelets to aggregating agents in vitro and can completely reverse experimentally produced platelet hypersensitivity [5].

High impact information on HALOFENATE

• We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas [6].
• We hypothesized that halofenate might be an insulin sensitizer, and we present data to suggest that halofenate is a selective peroxisome proliferator-activated receptor (PPAR)-gamma modulator (SPPARgammaM) [1].
• Halofenate did not alter serum TBG binding capacity [7].
• The effect of halofenate on beta adrenergic blockade by propranolol was studied in 4 subjects during chronic drug administration in a randomized, double-blind study [8].
• Clofibrate and halofenate reverse some of the abnormalities in vitro and the former drug, when administered for 6 weeks to patients with type IIa hyperlipoproteinemia decreases platelet sensitivity to ADP and epinephrine [9].

Biological context of HALOFENATE

• Halofenate--free acid (HFA), the major metabolite of the hypolipidemic drug, halofenate, inhibited platelet aggregation induced by collagen and sodium arachidonate and blocked the second phase of aggregation caused by ADP, thrombin and epinephrine in human platelet-rich plasma [10].

Associations of HALOFENATE with other chemical compounds

• Rats fed a fat-free diet containing no drug, 0.02% or 0.10% halofenate, or 0.25% clofibrate for 14 days were injected intravenously with equivalent amounts of either [2-3H]glycerol or [1(3)-3H]glycerol [11].
• Effects of halofenate on glucose tolerance in patients with hyperlipoproteinemia [12].
• While pyruvate dehydrogenase was inhibited in vitro, halofenate also inhibited the activety of various other isolated enzymes [13].
• Methods employing solvent extraction, thin-layer chromatography, gas-liquid chromatography, and UV spectrophotometry are described for the quantitative determination of halofenate, cyclobenzaprine and sulindac in rodent diet mixtures [14].
• Three highly reproducible experiments on drug interaction in normal human volunteers provided anomalous results: chronic halofenate administration shortened plasma antipyrine and bishydroxycoumarin half-lives but prolonged plasma warfarin half-lives [15].

Gene context of HALOFENATE

• The influence of Halofenate therapy on insulin and glucagon secretion was examined in the Zucker rat with genetic endogenous hyperlipemia [16].
• Coincident with the lipid lowering effects of Halofenate, the net change in the basal bihormonal axis favored glucagon, with the I/G molar ratio (Insulin/Glucagon) decreasing from 2.72 +/- 0.53 to 0.96 +/- 0.20 during treatment with this drug [16].

Analytical, diagnostic and therapeutic context of HALOFENATE

• Six-hour oral glucose tolerance tests were done during a control period and every 24 weeks over two years of halofenate treatment [12].

References