104700-95-0
Chemical Structure
Ganoderic acid K
- CAS No.: 104700-95-0
- Formula:C32H46O9
- Molecular Weight:574.70
IUPAC Name: (2R,6R)-6-((3S,7S,10S,12S,13R,14R,17R)-12-acetoxy-3,7-dihydroxy-4,4,10,13,14-pentamethyl-11,15-dioxo-2,3,4,5,6,7,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)-2-methyl-4-oxoheptanoic acid
InChIKey: OEHYQHPDUCRLMW-KSTZBSRVSA-N
SMILES: C[C@@H]([C@H]1CC([C@]2(C)[C@]1(C)[C@H](OC(C)=O)C(C3=C2[C@@H](O)CC4[C@]3(C)CC[C@H](O)C4(C)C)=O)=O)CC(C[C@H](C(O)=O)C)=O
Biological Activity: Ganoderic acid K is a triterpenoid compound. Ganoderic acid K can be isolated from Ganoderma lucidum. Ganoderic acid K inhibits ACE activity with an IC50 of 2.6×10-5 M. Ganoderic acid K exhibits direct, high-affinity binding to recombinant MD2 protein, with a Kd value of 0.47 μM. It potently inhibits LPS-induced release of TNF-α and IL-6. It reduces cerebral infarction volume and ameliorates neurological dysfunction in mice with ischemic stroke in the tMCAO model. Ganoderic acid K can be used in studies related to hypertension and ischemic stroke[1][2].
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Ganoderic acid K | Ganoderic acid K is a triterpenoid compound. Ganoderic acid K can be isolated from Ganoderma lucidum. Ganoderic acid K inhibits ACE activity with an IC50 of 2.6×10-5 M. Ganoderic acid K exhibits direct, high-affinity binding to recombinant MD2 protein, with a Kd value of 0.47 μM. It potently inhibits LPS-induced release of TNF-α and IL-6. It reduces cerebral infarction volume and ameliorates neurological dysfunction in mice with ischemic stroke in the tMCAO model. Ganoderic acid K can be used in studies related to hypertension and ischemic stroke. | |||||||||||||||||||||
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References
- [1]. Morigiwa A, et al. Angiotensin converting enzyme-inhibitory triterpenes from Ganoderma lucidum. Chem Pharm Bull (Tokyo). 1986 Jul;34(7):3025-8. [Content Brief]
- [2]. Ma A, et al. Ganoderic Acids Alleviate Neuroinflammation by Targeting Myeloid Differentiation Factor 2 for Ischemic Stroke Therapy. Exploration (Beijing). 2026;6(1):20240147. Published 2026 Feb 18. [Content Brief]
