2. Anti-infection Apoptosis Metabolic Enzyme/Protease Immunology/Inflammation NF-κB
  3. Antibiotic Bacterial Apoptosis Reactive Oxygen Species Bcl-2 Family NO Synthase COX TNF Receptor Interleukin Related
  4. Asperlin

Asperlin is an orally active marine-derived antibiotic with antifungal, anticancer, anti-inflammatory and anti-atherosclerotic activities. Asperlin induces apoptosis. Asperlin increases reactive oxygen species (ROS)- and DNA damage-associated G2/M phase arrest and ATM phosphorylation. Asperlin is effective in preventing HFD-induced obesity and modulating gut microbiota.

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Asperlin Chemical Structure

Asperlin Chemical Structure

CAS No. : 30387-51-0

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Description

Asperlin is an orally active marine-derived antibiotic with antifungal, anticancer, anti-inflammatory and anti-atherosclerotic activities. Asperlin induces apoptosis. Asperlin increases reactive oxygen species (ROS)- and DNA damage-associated G2/M phase arrest and ATM phosphorylation. Asperlin is effective in preventing HFD-induced obesity and modulating gut microbiota[1][2][3][4][5].

In Vitro

Asperlin (6-25 μM, 24-48 h) inhibits cell growth in a dose dependent manner, induces cleavage of caspase-3 and PARP and reduces Bcl-2, and induces cell apoptosis. N-acetyl-L-cysteine (HY-B0215, NAC) can block all the apoptotic effects of Asperlin in HeLa cells[1].
Aaperlin (6-25 μM, 24 h) increases ROS- and DNA damage-associated G2/M phase arrest and ATM phosphorylation, and can be significantly blocked by NAC or an ATM inhibitor KU-55933 (HY-12016) pretreatment[1].
Aaperlin (5-40 μM, 12 h) has anti-inflammatory effects in macrophages, suppresses LPS-induced iNOS and COX-2 expression, decreases TNF-α and IL-1β production in a dosedependent manner in both murine peritoneal macrophages and RAW264.7 macrophages[3].
Asperlin (500μg/ml, 1 d) effectively controls the development of tomato late blight and wheat leaf rust with a disease control value of 95%[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Cell Line: HeLa
Concentration: 6, 12.5, 25 μM
Incubation Time: 24, 48 h
Result: Increased ROS generation while little increase could be seen in the presence of NAC.
Cell growth was inhibited in dose dependent manner, but was restored in the presence of NAC.

Cell Cycle Analysis[1]

Cell Line: HeLa
Concentration: 6, 12, 25 μM
Incubation Time: 24 h
Result: Significantly increased G2/M phase cells.
Pretreatment with either NAC or KU-55933 significantly abrogated the G2/M arresting effect.
Phosphorylation of Chk2, cdc2 and cyclinB1 was found to be reduced by pretreatment of NAC and KU-99533

Apoptosis Analysis[1]

Cell Line: HeLa
Concentration: 25 μM
Incubation Time: 24, 48 h
Result: Induced caspase-3 activation and PARP cleavage as well as Bcl2 reduction, and the effect were completely blocked by NAC pretreatment to the cells.

Western Blot Analysis[1]

Cell Line: HeLa
Concentration: 6, 12, 25 μM
Incubation Time: 24 h
Result: Expression of cyclin A2 and cyclin B1 was increased.
Phosphorylation of Bcl-2 and of cdc2 which is inactive when phosphorylated at residues Thr-14 and Tyr-15, was increased. and cdc25C expression was reduced.
Induced the phosphorylation of both ATM and Chk2 in the cells without having any effect on p21.
In Vivo

Asperlin (40-80 mg/kg; p.o.; once daily for 12 weeks) effectively prevents the development of obesity, stimulates energy expenditure and modulates gut microbiota in high-fat diet (HFD)-fed mice[2].
Asperlin (80mg / kg; p.o.; once daily for 12 weeks) remarkably suppresses atherosclerotic plaque formation in the aorta, as revealed by the reduced aortic dilatation and decreased atherosclerotic lesion area in high-fat diet (HFD)-fed ApoE-/- mice[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J mice (8-weeks old, weighing 20-25g) were fed with a high-fat diet (HFD) to induce obesity[2]
Dosage: 40, 80 mg/kg
Administration: Oral gavage (p.o.), once daily for 12 weeks
Result: Showed lower body weight, and food intake was not varied.
Reduced the blood levels of total cholesterol (TC), triglycerides (TG) and low-density lipoprotein (LDL-c). Liver TC, TG contents and fat vacuoles were also substantially reversed.
Increased energy expenditure and enhanced thermogenic gene (PGC1α, UCP1, CIDEA, CPT1B, FATP1, CYTO-C) expression in adipose tissue.
Increased the diversity of the gut microbes. Significantly shifted the structure of the gut microbiota.
Animal Model: Male C57BL/6 J and C57BL/6 J ApoE−/− mice (6-8 weeks, weighting 20-25 g)[5]
Dosage: 80 mg/kg
Administration: Oral gavage (p.o.), once daily for 12 weeks
Result: Remarkably suppressed atherosclerotic plaque formation in aorta, reduced the white atherosclerotic lesions, effectively inhibited aortic dilatation in ApoE−/− mice.
Molecular Weight

212.20

Formula

C10H12O5
CAS No.
SMILES

CC(O[C@@H]1[C@@]([C@]2([H])[C@H](O2)C)([H])OC(C=C1)=O)=O
Structure Classification
Initial Source

Aspergillus caespitosus
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Keywords:

Asperlin30387-51-0AntibioticBacterialApoptosisReactive Oxygen SpeciesBcl-2 FamilyNO SynthaseCOXTNF ReceptorInterleukin RelatedNitric oxide synthasesNOSCyclooxygenaseTumor Necrosis Factor ReceptorTNFRILgut microbiotaobesityG2/MATMDNA-damageantibioticROSanti-inflammatoryantifungalanti-atherosclerotic activitiesanticancerInhibitorinhibitorinhibit

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