Hecogenin acetate 

Hecogenin acetate is an orally active steroid saponin aglycone with extensive biological activities. Hecogenin acetate inhibits the phosphorylation of NF-κB and p38 MAPK signaling pathways, antagonizes TRPA1/TRPM8 channels, inhibits the production of pro-inflammatory cytokines, and has anti-inflammatory and analgesic effects. Hecogenin acetate inhibits the production of ROS and the activation of NLRP3 inflammasome; downregulates the expression of MMP-2, and has neuroprotective and anti-tumor activities. Hecogenin acetate enhances gastric mucosal defense and promotes ulcer healing. Hecogenin acetate can be used in combination with certain antibiotics to regulate bacterial efflux pumps and restore antibiotic sensitivity^{[1][2][3][4][5]}.

Hecogenin acetate has only a very weak direct antibacterial activity with MIC values for S. aureus ATCC and E. coli ATCC of 645 μg/mL and 512 μg/mL respectively^[3].
Hecogenin acetate (1-150 μM, 24 h) has no significant effect on the viability of A549 cells when the concentration was lower than 75 μM, but at higher concentrations it reduces the viability of A549 cells^[4].
Hecogenin acetate (50 μM, 24 h) reverses the cell membrane damage, ROS production, and increased activities of catalase (CAT) and superoxide dismutase (SOD) caused by H₂O₂ in A549 cells^[4].
Hecogenin acetate (25-100 μM, 24-72 h) induces G0/G1 phase cell cycle arrest and cellular senescence by inhibiting the ERK1/2 signaling pathway and reducing the expression of MMP-2^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Hecogenin acetate (20 mg/kg, i.g., once daily for 8 or 15 days) significantly alleviates chronic inflammatory pain and neuropathic pain in mice^[1].
Hecogenin acetate (5-25 mg/kg, i.p., single dose or once daily for 7 days) inhibits the expression of the aldosterone synthase (CYP11B2) gene, thereby exerting a diuretic effect in rats^[2].
Hecogenin acetate (2.5-10 mg/kg, p.o., single dose or once daily for 7 days) exhibits significant protective effects against acute gastric mucosal injury induced by various chemical substances (anhydrous ethanol, acidified ethanol) and pathological processes (ischemia-reperfusion) in rodent models^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

472.66

C₂₉H₄₄O₅

915-35-5

Solid

White to yellow

[H][C@]1(O[C@@]2(OC[C@H](C)CC2)[C@@H](C)[C@@]1([C@]34C)[H])C[C@@]3([H])[C@]5([H])CC[C@@]6([H])C[C@@H](OC(C)=O)CC[C@]6(C)[C@@]5([H])CC4=O

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Santos Passos FR, et al. Role of peripheral and central sensitization in the anti-hyperalgesic effect of hecogenin acetate, an acetylated sapogenin, complexed with β-cyclodextrin: Involvement of NFκB and p38 MAPK pathways. Neuropharmacology. 2021 Mar 15;186:108395.  [Content Brief]

  [2]. Alamoudi AJ, et al. Diuretic effects of Hecogenin and Hecogenin acetate via aldosterone synthase inhibition. Saudi Pharm J. 2024 Jul;32(7):102105.  [Content Brief]

  [3]. Santos Araújo NJ, et al. Evaluation of the antibacterial activity of hecogenin acetate and its inhibitory potential of NorA and MepA efflux pumps from Staphylococcus aureus. Microb Pathog. 2023 Jan;174:105925.  [Content Brief]

  [4]. Gasparotto J, et al. Hecogenin acetate inhibits reactive oxygen species production and induces cell cycle arrest and senescence in the A549 human lung cancer cell line. Anticancer Agents Med Chem. 2014;14(8):1128-35.  [Content Brief]

  [5]. Sousa AJC, et al. Antiulcerogenic and healing activity of hecogenin acetate in rodents. Naunyn Schmiedebergs Arch Pharmacol. 2023 Apr;396(4):759-769.  [Content Brief]