Alpha-mangostin targets multiple biological pathways. It inhibits the production of pro-inflammatory cytokines and modulates NF-κB and MAPK signaling pathways. The compound exhibits potent antioxidant activity through free radical scavenging. It induces apoptosis in cancer cells through mitochondrial pathways and inhibits cancer cell proliferation. Alpha-mangostin also demonstrates antimicrobial activity against various pathogens and shows neuroprotective effects.

α-Mangostin (α-Mangostin) suppresses IDH1-R132H but not IDH1. IDH1-R132H is inhibited by α-Mangostin (α-Mangostin). According to studies, the strongest core flipped structure is seen in α-Mangostin (α-Mangostin). α-Mangostin (α-Mangostin) preferentially stimulates the demethylation of trimethylated lysine residues in histone H3 and 5-methylcellulose (5mC) in IDH1 (+/R132H) MCF10A cells [1]. Cell proliferation was markedly and dose-dependently inhibited in cells treated with α-mangostin. Additionally, α-Mangosteen raises mitochondrial caspase-9, mitochondrial caspase-3, mitochondrial poly(ADP-ribose) polymerase (PARP), and pigmentogen Bax levels [2]. α-Mangostin (α-Mangostin) notably reduces fotoThe production of reactive oxygen species (ROS) and malondialdehyde (MDA) caused by light is inhibited by α-Mangostin (α-Mangostin) at 200 μM H2O2[3].
In vitro, alpha-mangostin exhibits potent antioxidant activity through free radical scavenging. It demonstrates anti-inflammatory effects by inhibiting the production of pro-inflammatory cytokines and modulating NF-κB and MAPK signaling. The compound shows anti-cancer activity by inducing apoptosis and inhibiting proliferation in various cancer cell lines. It also exhibits antimicrobial activity against bacteria and fungi, and shows neuroprotective effects in neuronal cell models.

By decreasing p53 expression in comparison to TAA_DMSO therapy, α-Mangostin (α-Mangostin) lowers the risk of liver fibrosis. Compared to DMSO alone, the therapy with α-Mangostin resulted in lower serum levels of the liver enzymes AST and ALT [4].
In vivo, alpha-mangostin has demonstrated anti-inflammatory and anticancer activities in animal models. It has been shown to inhibit tumor growth in xenograft models and reduce inflammation in various inflammatory disease models. The compound's antioxidant and neuroprotective effects have also been demonstrated in vivo. Further studies are ongoing to fully characterize its pharmacological effects and therapeutic potential.

For in vitro antioxidant assays, alpha-mangostin can be evaluated using DPPH, ABTS, or FRAP assays. The compound is incubated with radical solutions or ferric reducing agents, and the decrease in absorbance or increase in color is measured. Anti-inflammatory activity can be assessed by measuring inhibition of pro-inflammatory cytokine production in stimulated cells using ELISA.

For in vitro cell-based assays, alpha-mangostin is typically tested on cancer cell lines, immune cells, or neuronal cells. Cells are treated with the compound at various concentrations (typically 1-100 μM) for 24-72 hours. Cell viability is assessed using MTT or CCK-8 assays. Cytokine production is measured by ELISA. Apoptosis is evaluated by flow cytometry. Antimicrobial activity is assessed using broth microdilution assays. Signaling pathway modulation is assessed by Western blotting.

For in vivo animal experiments, alpha-mangostin is typically administered orally or intraperitoneally to mouse models of cancer, inflammation, or neurodegeneration. In cancer models, tumor volume is measured. In inflammation models, inflammatory markers are measured. Neuroprotective effects are assessed in neurodegeneration models. Histopathological examination of tissues is performed to evaluate efficacy and safety.

Pharmacokinetic data for alpha-mangostin are available from various studies. The compound has moderate oral bioavailability and undergoes extensive metabolism in the liver. It has a relatively long half-life and distributes to various tissues including the brain. Standard pharmacokinetic parameters including Cmax, Tmax, half-life, and AUC have been characterized in animal models.

Interactions
Membrane integrity alterations and inflammation play a crucial role in cardiovascular injury. This study investigated the beneficial effects of exogenous α-retropine on β-adrenergic catecholamine-induced cardiovascular toxicity, focusing particularly on the expression of membrane ATPases, lysosomal hydrolases, and inflammatory mediators TNF-α and cyclooxygenase-2 (COX-2) in albino rats. Two days after induction with isoproterenol (150 mg/kg body weight, intraperitoneal injection), the activities of serum and cardiac lysosomal hydrolases (β-D-glucuronidase, β-D-galactosidase, β-DN-acetylglucosidase, acid phosphatase, and cathepsin D) were significantly increased. Significantly elevated sodium and calcium levels and decreased potassium levels were observed in the hearts of rats treated with isoproterenol (ISO), along with abnormal activity of membrane-bound phosphatases (Na(+)-K(+) ATPase, Ca(2+) ATPase, and Mg(2+) ATPase). Western blotting was used to detect the expression of TNF-α and COX-2 in the heart. Results showed that the expression of TNF-α and COX-2 was significantly elevated in the hearts of ISO-poisoned rats. Pre-oral administration of α-mangosteen (200 mg/kg body weight) for 8 days significantly alleviated these abnormalities and restored TNF-α and COX-2 levels to near-normal levels, showing a significant difference compared to the ISO-poisoned group. In summary, α-mangosteen maintains the integrity of cardiomyocyte membranes and reduces the abnormal expression of TNF-α and COX-2 by effectively alleviating ISO-induced oxidative stress and cell damage. The restoration of normal cellular status confirms the cytoprotective effect of α-mangosteen. Cisplatin (CDDP) is a chemotherapeutic drug that can cause nephrotoxicity associated with oxidative/nitrosogenic stress. α-mangosteen (α-M) is a flavonoid compound extracted from mangosteen and possesses antioxidant and anti-inflammatory properties. This study aimed to evaluate the renal protective effect of α-M against CDDP-induced nephrotoxicity. α-M (12.5 mg/kg/day, by gavage) was administered continuously for 10 days (7 days before and 3 days after CDDP injection). On day 7, rats received a single injection of CDDP (7.5 mg/kg, intraperitoneal injection); rats were sacrificed 3 days later. α-M reduced renal dysfunction, structural damage, oxidative/nitrosation stress, decreased catalase expression, and increased levels of tumor necrosis factor α and transforming growth factor β mRNA. In summary, the renal protective effect of α-M against cisplatin-induced nephrotoxicity was associated with the reduction of oxidative/nitrosation stress, inflammation and fibrosis markers, and the maintenance of catalase activity. α-Daucusin, isolated from the bark of Garcinia mangostana L., was active against vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococcus aureus (MRSA), with minimum inhibitory concentrations (MICs) of 6.25 μg/mL and 6.25–12.5 μg/mL, respectively. Our research indicates that alpha-retropine has a synergistic effect with gentamicin (GM) against vancomycin-resistant enterococci (VRE), and with vancomycin hydrochloride (VCM) against methicillin-resistant Staphylococcus aureus (MRSA). Further studies have shown that alpha-retropine also exhibits partial synergistic effects with commercially available antibiotics such as ampicillin and minocycline. These findings suggest that alpha-retropine, used alone or in combination with gentamicin, may be helpful in controlling VRE and MRSA infections, and its combination with vancomycin may also be effective.
Toxicological data for alpha-mangostin indicate that the compound is generally well-tolerated at pharmacological doses. However, high doses may cause toxicity in some organ systems. Comprehensive toxicological studies have been performed, and the compound is considered to have a reasonable safety profile for research applications. The compound is classified as a research-grade reagent and is not for human use.

[1]. Discovery of α-mangostin as a novel competitive inhibitor against mutant isocitrate dehydrogenase-1. Bioorg Med Chem Lett. 2015 Dec 1;25(23):5625-31.

[2]. Antitumor and apoptosis-inducing effects of α-mangostin extracted from the pericarp of the mangosteen fruit (Garcinia mangostana L.) in YD-15 tongue mucoepidermoid carcinoma cells. Int J Mol Med. 2016 Apr;37(4):939-48.

α-Xanthocyanin belongs to the xanthones class of compounds with the structure 9H-xanthones, substituted with hydroxyl groups at positions 1, 3, and 6, a methoxy group at position 7, a carbonyl group at position 9, and isopentenyl groups at positions 2 and 8. It was isolated from the stem of hawthorn (Cratoxylum cochinchinense) and possesses antioxidant, antibacterial, and antitumor activities. It can be used as an antitumor agent, antibacterial agent, antioxidant, and plant metabolite. It belongs to the xanthones, phenols, and aromatic ethers.
Xanthocyanin is a plant/plant extract used in certain over-the-counter (OTC) products. It is not an approved drug.
α-Xanthocyanin has been reported to exist in Garcinia cowa, Garcinia merguensis, and other organisms with relevant data.
See also: Garcinia mangostana pericarp (partial).

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Therapeutic Uses
Xanthones; Protein kinase inhibitors
/Experimental Therapy/Mangosteen has a long history of medicinal use in Chinese and Ayurvedic medicine. Recently, α-dextrin, a compound isolated from mangosteen pericarp, has been shown to induce the death of various cancer cells in vitro. This prompted us to investigate the anti-tumor growth and anti-metastatic activity of α-dextrin in a mouse xenograft model of metastatic breast cancer with a p53 mutation. This p53 mutation induces a metastatic spectrum similar to that of human breast cancer. After inoculating homologous BALB/c mice with metastatic BJMC3879luc2 cells to induce breast tumors, α-dextrin was administered using a micro-osmotic pump at doses of 0, 10, and 20 mg/kg/day, respectively, and histopathological examination was performed. In vitro experiments were also conducted to explore the anti-tumor mechanism of α-dextrin. The results showed that, compared with the control group, the in vivo survival rate of the 20 mg/kg/day α-dextrin group was significantly improved, and the tumor volume and the number of lymph node metastases were significantly reduced. The 20 mg/kg/day α-dextrin group also showed a significant increase in apoptosis levels in mouse mammary tumors, accompanied by increased expression of active caspase-3 and caspase-9. Furthermore, this dose group also showed decreased microvessel density and a reduced number of dilated lymphatic vessels containing intraluminal tumor cells in breast cancer tissue. In vitro experiments demonstrated that α-dextrin can induce mitochondrial-mediated apoptosis and inhibit the G1 and S phases of the cell cycle. Since Akt phosphorylation activation plays a central role in various carcinogenic processes, including cell proliferation, anti-apoptotic cell death, angiogenesis, and metastasis, we also investigated the effects of α-dextrin on Akt phosphorylation levels in vitro and in vivo. Quantitative analysis and immunohistochemical results showed that α-retropine significantly reduced the level of phosphorylated Akt-threonine 308 (Thr308) in breast cancer cell cultures and in vivo breast cancer tissues, but had no effect on the level of serine 473 (Ser473). Since lymph node metastasis is the most important prognostic factor for breast cancer patients, the anti-metastatic activity of α-retropine detected in p53-mutant breast cancer in this study may have specific clinical application value. Furthermore, α-retropine may have chemopreventive effects and/or may serve as adjuvant therapy or a complementary alternative to breast cancer treatment.
/Experimental Therapy/ This study aimed to test the activity of α-retropine against Candida albicans (the most important microorganism causing oral candidiasis) and compare its activity with clotrimazole and nystatin. The results showed that α-retropine was effective against Candida albicans, with a minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MFC) of 1000 and 2000 μg/mL, respectively. Alpha-retropine exhibits superior antifungal activity against Candida albicans compared to clotrimazole and nystatin. The cytotoxicity of α-retropine was determined, and a concentration of 4000 μg/mL was found to be non-toxic to human gingival fibroblasts within 480 minutes. Alpha-retropine's potent antifungal activity and low toxicity make it a promising drug for the treatment of oral candidiasis.
/Experimental Therapy/ Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of β-sheet-rich amyloid oligomers or fibrils, which are associated with cytotoxicity in the brain. Inhibiting Aβ accumulation may be a feasible therapeutic strategy to slow and/or halt the progression of AD. This article reports that the mangosteen polyphenol xanthones derivative α-dextrin (aM) can attenuate, in a concentration-dependent manner, the neurotoxicity induced by Aβ-(1-40) or Aβ-(1-42) oligomers (EC50 values of 3.89 nM and 4.14 nM, respectively) in primary rat cerebral cortical neurons, manifested as decreased cell viability and impaired neurite growth. Molecular docking and kinetic simulations suggest that aM may bind to Aβ and stabilize its α-helical conformation. Western blot analysis using oligomer-specific antibodies revealed that aM can directly dissociate Aβ-(1-40) and Aβ-(1-42) oligomers. Thioflavin T fluorescence assays and electron microscopy further confirmed that aM can inhibit fibril formation and disrupt existing fibrils. In summary, these results indicate that aM can inhibit and dissociate Aβ aggregation, which may help alleviate Aβ oligomer-induced neurotoxicity. Therefore, aM may be a highly promising candidate drug for the treatment of Alzheimer's disease (AD)...
Alpha-mangostin is a research-use only compound and has not been approved for clinical applications. It is one of the most studied xanthones from Garcinia mangostana (mangosteen). Its molecular weight and formula are well-characterized. It is available from various research chemical suppliers. The compound continues to be actively studied for its potential therapeutic applications in various diseases.

C24H26O6

410.4596

410.172

C, 70.23; H, 6.38; O, 23.39

6147-11-1

beta-Mangostin; 20931-37-7

5281650

Yellow solid solid

1.3±0.1 g/cm3

640.1±55.0 °C at 760 mmHg

182ºC

220.3±25.0 °C

0.0±2.0 mmHg at 25°C

1.624

5.45

3

6

5

30

677

0

O1C2C([H])=C(C(C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])=C(C=2C(C2=C1C([H])=C(C(=C2C([H])([H])/C(/[H])=C(\C([H])([H])[H])/C([H])([H])[H])OC([H])([H])[H])O[H])=O)O[H])O[H]

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

1,3,6-trihydroxy-7-methoxy-2,8-bis(3-methylbut-2-enyl)xanthen-9-one

NSC 27593; NSC 139154; NSC 30552; Alpha-Mangostin; NSC27593; NSC139154; NSC30552

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~110 mg/mL (~267.99 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: ≥ 2.75 mg/mL (6.70 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 27.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)