Olumacostat glasaretil is a small molecule inhibitor of acetyl coenzyme A carboxylase (ACC). It has been used in trials studying the treatment of Acne Vulgaris.

乙酰辅酶A羧化酶控制脂肪酸生物合成的首个、限速步骤。Olumacostat glasaretil抑制初级和转化的人类皮脂细胞中的去新生脂质合成。在3 μM的浓度下，Olumacostat glasaretil将脂肪酸合成降至基线水平或以下。使用20 μM Olumacostat glasaretil处理的SEB-1细胞培养物，与对照样本相比，14C-醋酸掺入水平降低了85%-90%。在3 μM浓度下，Olumacostat glasaretil平均将皮脂细胞中的三酰甘油、胆固醇/蜡酯、二酰甘油、胆固醇及磷脂水平从对照值分别降低了约86%、57%、51%、39%和37%[1]。

Olumacostat glasaretil是5-(tetradecyloxy)-2-furoic acid (TOFA)的前药，旨在提高体内递送效率。局部应用olumacostat glasaretil能显著减小仓鼠耳部皮脂腺大小，而TOFA则不能。HPLC分析显示，olumacostat glasaretil处理后，测试动物的ACC水平增加，乙酰辅酶A与自由辅酶A的比率上升，这暗示着脂肪酸氧化增加，这些变化与ACC抑制一致。Matrix-assisted laser desorption/ionization (MALDI)成像揭示，OG涂抹在约克郡猪耳朵上，相较于周围真皮，会积聚于皮脂腺中。到第12周，OG治疗在炎症性和非炎症性病变的基线减少方面及患者在研究者全球评估得分中达到或超过2级改善方面，显示出比对照组更大的减少。

Primary human sebocytes are grown to confluence in 96-well plates in sebocyte growth medium and stimulated with 1 μM human insulin and 1 μM liver X receptor (LXR) agonist T0901317 in the presence of increasing concentrations of TOFA or olumacostat glasaretil in culture medium containing 0.1% DMSO. After 24 hours, stimulation/treatment medium is removed and test articles are reapplied in labeling medium containing [14C]-acetate. Following an additional 16 hours, cells are harvested using trypsin/EDTA. Lipid extracts are prepared and the amount of [14C]-acetate incorporation is determined by liquid scintillation as a measure of de novo fatty acid synthesis[1].