915-35-5

Usage

Uses

Used in Veterinary Medicine:
Hecogenin acetate is used as an anthelmintic agent for the treatment of nematode infections in goats. It effectively reduces the percentage of mobile larvae in fecal cultures containing Haemonchus, Oesophagostomum, and Trichostrongylus nematodes, with an EC50 of 0.49 mg/ml.
Used in Pain Management:
Hecogenin acetate is used as an antinociceptive agent for the management of pain and hyperalgesia in mice. It inhibits the development of mechanical hyperalgesia induced by carrageenan, TNF-α, dopamine, and prostaglandin E2 (PGE2). Additionally, it increases latency to tail withdrawal in the tail flick test and has no effect on motor performance in the rotarod test when administered at a dose of 40 mg/kg.
Used in Pharmaceutical Research:
As a derivative of hecogenin, hecogenin acetate is used in pharmaceutical research for the development of new drugs and therapies. Its wide spectrum of pharmacological activities, including antinociceptive properties, make it a valuable compound for exploring potential applications in various medical fields.

Purification Methods

Crystallise the acetate from MeOH. [Beilstein 19 IV 2583.]

InChI:InChI=1/C29H44O5/c1-16-8-11-29(32-15-16)17(2)26-24(34-29)13-23-21-7-6-19-12-20(33-18(3)30)9-10-27(19,4)22(21)14-25(31)28(23,26)5/h16-17,19-24,26H,6-15H2,1-5H3/t16?,17-,19-,20?,21?,22?,23?,24?,26?,27?,28?,29?/m0/s1

Upstream product

• 108-24-7 acetic anhydride 
• 467-55-0 hecogenin 
• 5996-01-0 botogenin acetate 
• 10005-61-5 cyclopseudohecogenin acetate 
• 64-19-7 acetic acid 
• 121009-65-2 (23S,25R)-3β,11β-diacetoxy-23-bromo-5α-spirostan-12-one 
• 109-99-9 tetrahydrofuran 
• 67-56-1 methanol 
• 124-41-4 sodium methylate 

Downstream Products

• 545-77-7 3β,12β-dihydroxy-(25R)-5α-spirostane 
• 545-77-7 3β,12α-dihydroxy-(25R)-5α-spirostane 
• 11005-20-2 Pseudohecogenin 
• 4947-81-3 (23S,25R)-3β-acetoxy-11β,23-dibromo-5α-spirostan-12-one 
• 4947-81-3 (23R,25R)-3β-acetoxy-11α,23-dibromo-5α-spirostan-12-one 
• 5130-60-9 3β-acetoxy-11α,23α-dibromo-12-oxo-(25R)-5α-spirostane 
• 467-55-0 hecogenin 
• 3514-26-9 Δ⁹⁽¹¹⁾-22-isoallospirosten-3β-ol-12-one 
• 86023-87-2 3β,12β-dihydroxy-11-oxo-(25R)-5α-spirostane 
• 241465-96-3 Acetic acid (2S,4aS,4bS,6aS,6bR,9aS,10aS,10bR,12aS)-8-((R)-4-iodo-3-methyl-butyl)-4a,6a,7-trimethyl-6-oxo-2,3,4,4a,4b,5,6,6a,6b,9a,10,10a,10b,11,12,12a-hexadecahydro-1H-9-oxa-pentaleno[2,1-a]phenanthren-2-yl ester 
• 241465-87-2 Acetic acid (3S,5S,8R,9S,10S,13S,14S)-17-((1S,5R)-1,5-dimethyl-2-oxo-cyclohexyl)-10,13-dimethyl-12-oxo-2,3,4,5,6,7,8,9,10,11,12,13,14,15-tetradecahydro-1H-cyclopenta[a]phenanthren-3-yl ester 
• 943000-40-6 C₄₁H₄₈N₂O₁₀ 
• 943000-39-3 C₄₁H₄₈N₂O₁₀ 
• 943000-41-7 C₄₁H₅₀N₂O₁₀ 

Relevant academic research and scientific papers

Effects of hecogenin and its possible mechanism of action on experimental models of gastric ulcer in mice

This study investigates the gastroprotective effects of hecogenin, a steroid saponin isolated from Agave sisalana, on experimental models of gastric ulcer. Male Swiss mice were used in the models of ethanol- and indometacin-induced gastric ulcer. To clarify the hecogenin mechanism of action, the roles of nitric oxide (NO), sulfhydryls (GSH), K+ATP channels and prostaglandins were also investigated, and measurements of lipid peroxidation (TBARS assay) and nitrite levels in the stomach of hecogenin-treated and untreated animals were performed. Furthermore, the effects of hecogenin on myeloperoxidase (MPO) release from human neutrophils were assessed in vitro. Our results showed that hecogenin (3.1, 7.5, 15, 30, 60 and 90 mg/kg, p.o.) acutely administered, before ethanol or indomethacin, exhibited a potent gastroprotective effect. Although the pretreatments with L-NAME, an iNOS inhibitor, and capsazepine, a TRPV1 receptor agonist, were not able to reverse the hecogenin effect, this was reversed by glibenclamide, a K +ATP blocker, and indomethacin in the model of ethanol-induced gastric lesions. The hecogenin pretreatment normalized GSH levels and significantly reduced lipid peroxidation and nitrite levels in the stomach, as evaluated by the ethanol-induced gastric lesion model. The drug alone increased COX-2 expression and this effect was further enhanced in the presence of ethanol. It also decreased MPO release and significantly protected the gastric mucosa. In conclusion, we showed that hecogenin presents a significant gastroprotective effect that seems to be mediated by K +ATP channels opening and the COX-2/PG pathway. In addition, its antioxidant and anti-inflammatory properties may play a role in the gastroprotective drug effect.

Synthesis of betamethasone from the waste of Thai Agave sisalana

Synthesis of betamethasone from waste of Thai A. sisalana is described. Copyright Taylor & Francis Group, LLC.

Concurrent ring opening and halogenation of spiroketals

Ring opening of various spiroketals with triphenylphosphine dihalides under neutral conditions produced ω-halo-enolethers in good to excellent yield. The method transformed even the very stable spiroketal of hecogenin acetate at temperatures below any previously reported for such isomerative opening.

TRANSFORMATIONS OF SOLASODINE AND DERIVATIVES OF HECOGENIN BY CUNNINGHAMELLA ELEGANS

Incubation of (25R)-5α-spirostane-3β,12β-diol (rickogenin) with the fungus Cunninghamella elegans led to the formation of (25R)-7β,12β-dihydroxy-5α-spirostan-3-one, (25R)-5α-spirostan-3β,7β,12β-triol and (25R)-5α-spirostan-3β,7α,12α-triol.Incubation of (25R)-5α-spirostan-3,12-dione (hecogenone) with the same fungus gave rise to (25R)-5α-spirostan-3,7,12-trione.When the (22R,25R)-spirosolane, solasod-5-en-3β-ol (solasodine) was incubated with C. elegans, solasod-5-ene-3β,7β-diol, solasod-5-ene-3β,7α-diol and 3β-hydroxysolasod-5-en-7-one were produced.In contrast, incubation of solasodine with Penicillium patulum gave solasod-4-en-3-one and the 6-methylsalicylic acid salt of solasodine.