Monascuspiloin
Based on 1 Customer Validation
Monascuspiloin (Monascinol) is an orally active compound extracted from red mold-fermented rice, with multiple biological activities including anti-androgenic, anti-inflammatory, hypolipidemic, and anti-cancer properties. Monascuspiloin attenuates the PI3K/Akt/mTOR signaling pathway, enhances AMPK phosphorylation, downregulates FASN/SREBP2, induces apoptosis, G2/M phase arrest and autophagy in prostate cancer cells, interferes with dihydrotestosterone-receptor binding, enhances radiation-induced DNA damage, stimulates endoplasmic reticulum stress, and alleviates hepatic oxidative stress. Monascuspiloin regulates hepatic metabolic pathways and modulates the expression of genes and proteins related to hepatic lipid metabolism. Monascuspiloin can be used in studies related to prostate cancer and alcoholic liver injury.
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- Purity : 95%
- CAS No.: 1011244-19-1
- 화학식: C21H28O5
- 분자량:360.44
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보관:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
IC50 & Target
[1]|
Caspase 3 |
In Vitro
Monascuspiloin (compound MP) (5-200 μM; 24-48 h) inhibits the viability of both human androgen-dependent LNCaP and androgen-independent PC-3 prostate cancer cells with similar potency, showing IC50 values of 44.97 μM and 46.96 μM respectively after 48 h of treatment[1].
Monascuspiloin (50 μM;6-48 h) induces sub-G0/G1 accumulation (a marker of apoptosis) in human androgen-dependent LNCaP prostate cancer cells and G2/M arrest in human androgen-independent PC-3 prostate cancer cells[1].
Monascuspiloin (50 μM; 48 h) preferentially induces apoptosis in human androgen-dependent LNCaP prostate cancer cells via caspase activation, while only weakly inducing apoptosis in human androgen-independent PC-3 prostate cancer cells[1].
Monascuspiloin (50 μM; 6-48 h) induces apoptosis in human androgen-dependent LNCaP prostate cancer cells via inactivation of the Akt/mTOR pathway, while inducing autophagic and apoptotic cell death in human androgen-independent PC-3 prostate cancer cells via activation of the AMPK pathway[1].
Monascuspiloin (50 μM; 48 h) preferentially induces autophagic cell death in human androgen-independent PC-3 prostate cancer cells, which sensitizes cells to apoptosis, while inducing only minimal autophagy in human androgen-dependent LNCaP prostate cancer cells[1].
Monascuspiloin (MP) (5-45 μM; 48 h) reduces the viability of human prostate cancer PC-3 cells in a concentration-dependent manner[2].
Monascuspiloin (15-25 μM; in combination with ionizing radiation) enhances the radiation sensitivity of human prostate cancer PC-3 cells, reducing clonogenic survival fractions compared to ionizing radiation alone[2].
Monascuspiloin (25 μM; 48 h) enhances ionizing radiation-induced DNA damage in human prostate cancer PC-3 cells, significantly increasing comet tail length compared to either treatment alone; it induces endoplasmic reticulum stress in human prostate cancer PC-3 cells; it inhibits the Akt/mTOR signaling pathway in human prostate cancer PC-3 cells; and it induces autophagy in human prostate cancer PC-3 cells. These effects are significantly enhanced when combined with ionizing radiation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:5, 25, 50, 100, 200 μM
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Incubation Time:24 h; 48 h
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Result:Significantly decreased cell viability in both LNCaP and PC-3 cells in a concentration- and time-dependent manner.
Exhibited IC50 values of 44.97 μM for LNCaP cells and 46.96 μM for PC-3 cells after 48 h of treatment.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM
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Incubation Time:12, 24, 48 h
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Result:Raised sub-G0/G1 population and reduced G0/G1 and G2/M fractions in LNCaP cells at 24 h and 48 h.
Slightly elevated sub-G0/G1 proportion and triggered prominent G2/M cell cycle arrest in PC-3 cells across 12 h, 24 h and 48 h.
Upregulated cyclin B and phosphorylated cdc2 in PC-3 cells in a time-dependent manner with no such change in LNCaP cells.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM
20 μM Z-VAD-FMK (HY-16658B) -
Incubation Time:6, 12, 24, 48 h; 1 h (Z-VAD-FMK pretreatment)
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Result:Triggered time-dependent apoptosis in LNCaP cells verified by DNA fragmentation, elevated Annexin V positivity, activated caspase-3, upregulated pro-apoptotic Bax/Bad and downregulated anti-apoptotic Bcl-2/Bcl-xl.
Pretreatment with Z-VAD-FMK weakened this apoptosis and rescued cell viability in LNCaP cells.
Exerted only weak pro-apoptotic effect on PC-3 cells with negligible shifts in Bax, Bad and Bcl-xl; Z-VAD-FMK failed to reverse the viability decline in PC-3 cells.
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Cell Line:human androgen-dependent LNCaP prostate cancer cells, human androgen-independent PC-3 prostate cancer cells
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Concentration:50 μM; 2.5 mM 3-Methyladenine (HY-19312)
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Incubation Time:48 h; 1 h (3-Methyladenine pretreatment)
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Result:Induced autophagy in PC-3 cells, as evidenced by the presence of autophagic vacuoles via electron microscopy, increased AVOs (35% of cells after 48 h), and increased expression of LC3-II, Atg5, and Beclin 1.
Attenuated monascuspiloin-induced autophagy and apoptosis, and reversed cell viability loss in PC-3 cells when pretreated with 3-Methyladenine.
Induced minimal autophagy in LNCaP cells, with only 15% of cells showing AVOs after 48 h of treatment.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:5 μM, 15 μM, 25 μM, 35 μM, 45 μM
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Incubation Time:48 h
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Result:Reduced PC-3 cell viability in a concentration-dependent manner.
Decreased cell viability to 60% at 25 μM for 48 h.
Resulted in significantly lower cell viability at 15, 25, 35, and 45 μM.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:25 μM (alone or in combination with 4 Gy ionizing radiation)
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Incubation Time:48 h
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Result:Upregulated IRE1α and phosphorylated eIF2α expression relative to untreated groups as single treatment.
Amplified the upregulation of the two proteins upon combination with 4 Gy radiation, indicating aggravated ER stress.
Suppressed phosphorylation of Akt, mTOR and p70S6K alone versus untreated controls.
Strengthened the inhibitory effect on the phosphorylation of these kinases under combined 4 Gy irradiation, with total protein expression unaltered.
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Cell Line:human prostate cancer PC-3 cells
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Concentration:25 μM (alone or in combination with 4 Gy ionizing radiation)
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Incubation Time:48 h
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Result:Raised the proportion of acridine orange-positive AVOs to roughly 22% as single agent, matching the effect of separate 4 Gy irradiation.
Boosted the percentage of AVOs to approximately 42% under combined treatment with 4 Gy radiation, far exceeding single treatment groups.
Triggered abundant autophagic vacuoles and autolysosomes in co-treated cells without apoptotic chromatin condensation.
Upregulated LC3-II, p62/SQSTM1 and Atg5-12 expression after combined 4 Gy radiation exposure versus individual treatments.
In Vivo
Monascuspiloin (MP) (1 mg/kg; three times per week; for 2 weeks) alone inhibits the growth of prostate tumors in nude mice; when combined with 6 Gy ionizing radiation, it increases the tumor growth inhibition rate and significantly prolongs the tumor growth delay time[2].
Monascuspiloin (10 mg/kg; p.o.; once daily; for 6 consecutive weeks) alleviates alcoholic liver injury in male Kunming mice by improving liver function, reducing oxidative stress, regulating lipid metabolism, restoring intestinal flora balance, modulating hepatic metabolic pathways, and regulating hepatic gene and protein expression[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/C-nu/nu nude mice (male, 5 weeks old)[1]
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Dosage:40 mg/kg; 120 mg/kg
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Administration:i.p.; 3 times weekly; 6 total injections
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Result:Inhibited tumor growth dose-dependently by 63% and 74% on day 18, lengthened tumor quadrupling and growth delay time, reduced tumor weight, suppressed proliferation marker PCNA, activated apoptosis via cleaved caspase 3, upregulated multiple autophagy proteins, and caused no weight loss or evident toxicity.
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Animal Model:BALB/cAnN.Cg-Foxn1nu/CrlNarl (male, 6-8 weeks old, subcutaneous injection of 2×106 PC-3 human prostate cancer cells)[2]
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Dosage:1 mg/kg (monotherapy); 1 mg/kg (combined with 6 Gy ionizing radiation)
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Administration:three times per week; 2 weeks
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Result:Inhibited tumor growth by 42.5% on day 10, prolonging tumor volume quadrupling time to 20.7 days and growth delay to 10.4 days.
Enhanced antitumor effect with 6 Gy radiation to 71.4% inhibition, extending quadrupling time to 62.6 days and delay to 52.3 days.
Reduced tumor weight more effectively than single treatment alone.
Elevated LC3 and p62 levels in tumor tissues versus monotherapy groups.
Caused no weight loss and exhibited no obvious systemic toxicity.
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Animal Model:Kunming mice (male, six-week-old, specific pathogen-free)[3]
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Dosage:10 mg/kg
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Administration:p.o.; daily; 6 weeks
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Result:Corrected alcohol-caused weight loss and lowered elevated liver index by 13.01%.
Lowered serum TC, TG, LDL-C, ALT and AST while raising serum HDL-C.
Decreased hepatic TC, BAs, MDA and LDH, and boosted hepatic GSH, CAT, SOD and ADH.
Alleviated hepatic steatosis and ameliorated liver pathological lesions.
Elevated multiple fecal short-chain fatty acids and repaired alcohol-triggered intestinal mucosal injury.
Regulated the relative abundance of multiple intestinal flora genera.
Remodeled 75 hepatic metabolites and interfered with several key metabolic pathways.
Modulated the transcription of lipid metabolism, detoxification, antioxidant and inflammatory-related genes.
Upregulated LDLr, CPT-1, Nrf-2, NQO1 and HO-1 protein expression and suppressed SREBP-1 protein level.
- Western Blot
- RNA extraction experimental
- Annexin V plus membrane-impermeant dye apoptosis staining
- ROS/oxidative-stress fluorescent staining
- Protocol for Cell Cycle
- Research Protocol for Inflammation-related Diseases
- Kinase activity and phosphorylation assays
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Flow cytometric DNA-content cell-cycle staining
- Autophagy
- Apoptosis Solutions
- Protocol for Kinase activity and phosphorylation assays
- Lysosome and acidic-vesicle live-cell staining
- Macroautophagy Solutions
- Genotoxicity/Mutagenicity Study
Chemical Information
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CAS No. 1011244-19-1
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Appearance Solid
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분자량 360.44
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화학식 C21H28O5
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Color Yellow to orange
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SMILES
C[C@]12[C@@](CC3=C(COC(/C=C/C)=C3)C2=O)([H])[C@H](C(O1)=O)[C@@H](O)CCCCC
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Synonyms
Monascinol
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Structure Classification
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Initial Source
Monascus pilosus BCRC 38093-FERMENTED RICE
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
순도&문서
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Data Sheet (297 KB)
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SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
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Handling Instructions (2659 KB)
References
[1]. Chen RJ, et al. Monascuspiloin induces apoptosis and autophagic cell death in human prostate cancer cells via the Akt and AMPK signaling pathways. Journal of agricultural and food chemistry. 2012 Jul 25;60(29):7185-93. [Content Brief]
[2]. Chiu HW, et al. Monascuspiloin enhances the radiation sensitivity of human prostate cancer cells by stimulating endoplasmic reticulum stress and inducing autophagy. PloS one. 2012;7(7):e40462. [Content Brief]
[3]. Wu L, et al. Monascuspiloin from -Fermented Red Mold Rice Alleviates Alcoholic Liver Injury and Modulates Intestinal Microbiota. Foods (Basel, Switzerland). 2022 Sep 30;11(19):3048. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Monascuspiloin Related Classifications
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