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Details

Stereochemistry ACHIRAL
Molecular Formula C24H26O6
Molecular Weight 410.4596
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of MANGOSTIN

SMILES

COC1=C(CC=C(C)C)C2=C(OC3=C(C2=O)C(O)=C(CC=C(C)C)C(O)=C3)C=C1O

InChI

InChIKey=GNRIZKKCNOBBMO-UHFFFAOYSA-N
InChI=1S/C24H26O6/c1-12(2)6-8-14-16(25)10-19-21(22(14)27)23(28)20-15(9-7-13(3)4)24(29-5)17(26)11-18(20)30-19/h6-7,10-11,25-27H,8-9H2,1-5H3

HIDE SMILES / InChI

Description

α-Mangostin is a bioactive compound isolated from Garcinia mangostana L. known as the queen of fruits. Traditionally, numerous parts of G. mangostana have been utilized to treat various ailments such as abdominal pain, food allergies, arthritis, leucorrhoea, gonorrhea, diarrhea, and chronic ulcer. Experiments on animal have revealed that alpha-mangostin, an acid sphingomyelinase inhibitor, plays a protective role in diabetic neuropathy by relieving ER stress induced-renal cell apoptosis. Besides, it used against gastric ulcer, but this study was discontinued. α-Mangostin is also a histamine H1 receptor antagonist and is a specific inhibitor of lysine-specific demethylase 1 (LSD1), which has been reported to be overexpressed in several human cancers. α-mangostin has anti-carcinogenic effects against several cancers, including breast, colorectal cancers, and renal cell carcinoma. Thus, α-mangostin can be used to produce more potent LSD1 inhibitors with potential anticancer activity.

CNS Activity

Originator

Approval Year

Targets

Primary TargetPharmacologyConditionPotency
14.1 µM [IC50]
2.81 µM [IC50]

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Unknown
Palliative
Unknown
Primary
Unknown

PubMed

Sample Use Guides

In Vivo Use Guide
type 2 diabetic rats: Alpha-mangostin (200 mg/kg BW/day) were fed followed by i.p. injection of streptozotocin
Route of Administration: Oral
In Vitro Use Guide
α-mangostin at 10 μg/ml significantly suppressed the expression and phosphorylation of key proteins implicated in NF-κB pathway and inhibited nucleus translocation of p65. These changes led to increased apoptosis and proliferation inhibition of HFLS-RA cells.