2. PI3K/Akt/mTOR MAPK/ERK Pathway NF-κB
  3. PI3K Akt mTOR p38 MAPK NF-κB
  4. Calebin A

Calebin A is a PI3K/Akt/mTOR, MAPK, and NF-κB inhibitor with oral effectiveness. Calebin A can block the autophagy-repressive, inhibiting apoptosis. Calebin A has anti-tumor activity by epigenetic regulation. Calebin A suppresses adipogenesis, modulates thermogenesis, and enriches gut probiotics. Calebin A can be used in research on osteoarthritis, Alzheimer's disease, type 2 diabetes, malignant peripheral nerve sheath tumors, and colorectal cancer.

For research use only. We do not sell to patients.

Calebin A

Calebin A Chemical Structure

CAS No. : 336784-82-8

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Based on 1 publication(s) in Google Scholar

Calebin A Related Antibodies

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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mTOR mTORC1 mTORC2

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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Description

Calebin A is a PI3K/Akt/mTOR, MAPK, and NF-κB inhibitor with oral effectiveness. Calebin A can block the autophagy-repressive, inhibiting apoptosis. Calebin A has anti-tumor activity by epigenetic regulation. Calebin A suppresses adipogenesis, modulates thermogenesis, and enriches gut probiotics. Calebin A can be used in research on osteoarthritis, Alzheimer's disease, type 2 diabetes, malignant peripheral nerve sheath tumors, and colorectal cancer[1][2][3][4][5].

In Vitro

Calebin A (5 μM) suppresses apoptosis and promotes autophagic Beclin-1 expression in primary canine chondrocytes cultured in an osteoarthritis environment[1].
Calebin A (5 μM) upregulates ECM and autophagy markers, downregulates inflammation, degradation, apoptosis, and mTOR/PI3K/Akt signaling in primary canine chondrocytes cultured in an osteoarthritis environment, with effects dependent on intact autophagy[1].
Calebin A inhibits colonosphere formation, proliferation, invasion/migration, and enhances apoptosis in HCT116, RKO, and SW480 colorectal cancer cells via modulation of TNF-β/NF-κB signaling and associated biomarkers[2].
Calebin A overcomes vincristine resistance, induces G2/M-phase arrest and apoptosis in SGC7901 gastric cancer cells via modulation of MAPK signaling and P-glycoprotein[2].
Calebin A reduces growth and viability of Sup-T1 lymphoma cells and modulates epigenetic enzymes (HAT, HDAC, PCAF)[2].
Calebin A down-regulates inflammation in canine tenocytes via NF-κB/Scleraxis signaling[2].
Calebin A (20 μM) suppresses adipogenesis and induces lipolysis in adipocytes, with lipolysis induced at 20 μM[2].
Calebin A (25 μM; 24 h) induces G2/M phase decrease and G1 phase increase in STS26T, S462-TY, ST8814, and T265 MPNST cells, arresting cell cycle progression[3].
Calebin A (12.5-25 μM) downregulates phosphorylated AKT, phosphorylated ERK1/2, survivin, hTERT, and acetylated histone H3 in MPNST cells[3].

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

Calebin A Related Antibodies

Cell Proliferation Assay[3]

Cell Line: S462-TY, ST8814, T265, STS26T MPNST cell lines; LinNF primary neurofibroma cells
Concentration: 6.25, 12.5, 25, 50, 100 μM
Incubation Time: 24 h
Result: Decreased viability of MPNST cell lines at 12.5-25 μM; reduced survival by less than 50% in all MPNST cell lines with 25 μM treatment; inhibited growth of primary neurofibroma cells.

Cell Cycle Analysis[3]

Cell Line: STS26T, S462-TY, ST8814, T265 MPNST cell lines
Concentration: 25 μM
Incubation Time: 24 h
Result: Decreased STS26T cells in G2/M phase from 12.6% to 11.4% and increased G1 phase from 73.6% to 74.6%; reduced S462-TY G2/M phase from 19.7% to 8.8%, ST8814 G2/M phase from 6.4% to 6.0%, and T265 G2/M phase from 23.1% to 18.3%.

Cell Proliferation Assay[5]

Cell Line: HCT116 colorectal cancer cells (co-cultured with MRC-5 fibroblasts and Jurkat T-lymphocytes in multicellular proinflammatory TME; or co-cultured with MRC-5 fibroblasts and 10 ng/ml TNF-β in TNF-β-TME)
Concentration: 1-5 μM (10 days treatments); 5 μM (4 h immunofluorescence assay)
Incubation Time: 10 days (MTT, colonosphere, invasion, Western blotting); 4 h (immunofluorescence)
Result: Dose-dependently inhibited HCT116 cell proliferation, with maximum inhibition at 5 μM. Reduced colonosphere formation and invasion dose-dependently. Decreased nuclear p65-NF-κB labeling to 21% in multicellular TME and 22% in TNF-β-TME at 5 μM after 4 h treatment. Increased apoptosis to 59% in multicellular TME and 48% in TNF-β-TME at 5 μM after 4 h treatment. Suppressed p65-NF-κB phosphorylation, NF-κB-regulated gene products (MMP-9, CXCR4, Ki-67, β1-integrin), and cancer stem cell markers (CD133, CD44, ALDH1) dose-dependently. Increased cleaved caspase-3 dose-dependently.
Parmacokinetics
Species Dose Route T1/2 CLtotal CLrenal CLhepatic
Rat[6] 20 mg/kg i.v. 3.43 μg/mL 61 L/h/kg 0.11 L/h/kg 60.9 L/h/kg
Rat[6] 100 mg/kg p.o. 1.18 μg/mL 11244.3 L/h/kg 0.274 L/h/kg 11244.0 L/h/kg
In Vivo

Calebin A (100 mg/kg/d; p.o.; daily; 90 days) is safe when administered orally to female and male Wistar rats for 90 days, with no observed toxicity[2].
Calebin A (500 mg/kg; oral; single dose ) exhibits pharmacokinetic properties including ~0.5% bioavailability, 1-3 hour serum half-life, and primarily non-renal excretion in male Sprague-Dawley rats[2].
Calebin A (100 mg/kg; i.p.; three times a week; 15 days) significantly reduces xenograft tumor size in a mouse MPNST model[3].
Calebin A (0.1-0.5%; dietary supplementation; daily; 12 weeks) exhibits dose-dependent anti-obesity effects in high-fat diet-induced obese mice by reducing body weight and blood glucose, restoring liver weight, enhancing adaptive thermogenesis, and modulating gut microbiota composition[4].

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

Animal Model: Balb/c nude (male, 4 weeks old, MPNST xenograft model with S462-TY cells)[3]
Dosage: 100 mg/kg
Administration: i.p.; three times a week; 15 days
Result: Significantly decreased xenograft tumor size two weeks post-treatment.
Animal Model: C57BL/6 (male, 4 weeks old, high-fat diet-induced obesity)[4]
Dosage: 0.1%; 0.5%
Administration: high-fat diet (HFD) supplementation; daily; 12 weeks
Result: Reduced body weight in a dose-dependent manner; lowered fasting blood glucose and liver weight to normal diet levels (0.5% dose); decreased weights of white, beige, and brown adipose tissues (0.5% dose); improved liver color by reducing lipid accumulation (0.5% dose); better maintained rectal temperature with a higher area under the curve for temperature change than the high-fat diet group during 4°C cold exposure (0.5% dose); reduced Firmicutes-to-Bacteroidetes ratio from 1.24 ± 0.29 to 1.03 ± 0.42 (0.5% dose); increased Verrucomicrobia phylum abundance from 0.002 ± 0.001 to 0.022 ± 0.02 (0.5% dose); enriched genera including Akkermansia, Butyricicoccus, Ruminiclostridium_9, and unidentified_Ruminococcaceae (0.5% dose).
Molecular Weight

384.38

Formula

C21H20O7
CAS No.
SMILES

COC(C=C1/C=C/C(OCC(/C=C/C2=CC(OC)=C(C=C2)O)=O)=O)=C(C=C1)O
Structure Classification
Initial Source
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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Calebin A Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Calebin A336784-82-8PI3KAktmTORp38 MAPKNF-κBPhosphoinositide 3-kinasePKBProtein kinase BMammalian target of RapamycinNuclear factor-κBNuclear factor-kappaBextracellular signal-regulated kinase (ERK)histone acetyltransferase (HAT)c-Jun N-terminal kinase (JNK)cyclooxygenase-2 (COX-2)MMP9Wistar ratsInhibitorinhibitorinhibit

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