Cat. No.: HY-N2942

Bisdemethoxycurcumin

Bisdemethoxycurcumin is an orally effective curcuminoid. Bisdemethoxycurcumin downregulates pro-inflammatory cytokines in macrophages by inhibiting the phosphorylation of PI3K/Akt and p38 MAPK. Bisdemethoxycurcumin relieves autophagy inhibition and promotes lipophagy to clear vascular smooth muscle foam cells by inhibiting the PDK1/Akt/mTOR pathway. Bisdemethoxycurcumin activates the cAMP/Epac/AMPKα axis and the NRF2/HO-1 antioxidant axis, thereby indirectly inhibiting the phosphorylation of NF-κB p65 and pro-inflammatory outputs such as IL-1β/IL-6/TNF-α, so as to alleviate pulmonary oxidative stress, inflammatory infiltration and pulmonary edema. Bisdemethoxycurcumin blocks NLRP3-mediated pyroptosis and protects cartilage extracellular matrix degradation by activating NRF2/HO-1. Bisdemethoxycurcumin also exerts a synergistic effect with potassium iodide against Candida.

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

CAS No.: 52328-96-8
Formula: C₁₉H₁₆O₄
Molecular Weight:308.33

Storage:

Please store the product under the recommended conditions in the Certificate of Analysis.

Bisdemethoxycurcumin Chemical Structure

CAS No.: 52328-96-8

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- In Vitro
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

Description

All PI3K Isoforms :

All Akt Isoforms :

All p38 MAPK Isoforms :

All mTOR Isoforms :

All AMPK Isoforms :

All Interleukin Related Isoforms :

All TNF Receptor Isoforms :

All NOD-like Receptor (NLR) Isoforms :

In Vitro

Bisdemethoxycurcumin stably binds to purified human SRC, EGFR, AKT1, and PIK3R1 proteins, with the strongest binding affinity to AKT1 (-9.2 kcal/mol)^[1].
Bisdemethoxycurcumin (1-256 μM; 24-48 h) exhibits no cytotoxicity against ATDC5 chondrocytes at concentrations ≤ 8 μM within 24 h or 48 h, with a 48 h CC₅₀ value of 14.62 μM^[2].
Bisdemethoxycurcumin (2-8 μM; 7 days) dose-dependently reverses TBHP-induced reduction in the area of ATDC5 chondrocytes after 7 days of high-density culture^[2].
Bisdemethoxycurcumin (2.5-40 μM; 48 h) shows no cytotoxicity against RAW264.7 cells at concentrations of 2.5 μM and 5 μM after 48 h of incubation, but induces significant cytotoxicity at concentrations ≥ 10 μM^[1].
Bisdemethoxycurcumin (2.5 μM; 25 h) inhibits LPS-induced phosphorylation of Akt, PI3K and p38 proteins in RAW264.7 cells, but has no effect on the phosphorylation of ERK1/2 or JNK^[1].
Bisdemethoxycurcumin exhibits favorable pharmacokinetic properties and targets the PI3K/AKT signaling pathway, in which PDK1 serves as a key potential mediator of its anti-atherosclerotic effects^[3].
Bisdemethoxycurcumin (2.5 μM; 25 h) reduces the mRNA expression levels of IL-6, IL-1β, TNF-α and MCP-1 in LPS (HY-D1056)-induced RAW264.7 cells^[1].
Bisdemethoxycurcumin (2-8 μM; 48 h) reverses TBHP-induced extracellular matrix (ECM) degradation in ATDC5 chondrocytes in a dose-dependent manner by upregulating type II collagen and aggrecan, and downregulating ADAMTS4 and MMP3^[2].
Bisdemethoxycurcumin (2-8 μM; 48 h) activates the Nrf2/HO-1 pathway in a dose-dependent manner, and inhibits pyroptosis in TBHP-stimulated ATDC5 chondrocytes by upregulating Nrf2 and HO-1, and downregulating NLRP3, GSDMD, Caspase 1 and IL-1β, with a treatment duration of 48 h^[2].
Bisdemethoxycurcumin (8 μM; 24 h) significantly reduces the TBHP-induced upregulation of ADAMTS5 and NLRP3 protein expressions in ATDC5 chondrocytes^[2].
Bisdemethoxycurcumin (10-40 μM; 12 h) reduces lipid accumulation in mouse aortic vascular smooth muscle cells stimulated by oxidized low-density lipoprotein (ox-LDL) (HY-NP013) and promotes cholesterol efflux^[3].
Bisdemethoxycurcumin (20 μM; 12 h) promotes autophagy and reduces lipid deposition in ox-LDL-stimulated mouse aortic vascular smooth muscle cells by inhibiting the PDK1/Akt/mTOR signaling pathway^[3].
The autophagy-promoting and lipid-lowering effects of Bisdemethoxycurcumin (20 μM; 12 h) in ox-LDL-stimulated mouse aortic vascular smooth muscle cells depend on the downregulation of PDK1^[3].
Bisdemethoxycurcumin (10 µmol; 18 h) inhibits LPS-induced inflammatory responses and oxidative stress in primary mouse peritoneal macrophages by suppressing NF-κB p65 activation and restoring the levels of redox balance markers^[4].
Bisdemethoxycurcumin (10 µmol; 18 h) protects primary mouse peritoneal macrophages against LPS-induced inflammation and oxidative stress by activating AMPKα^[4].
Combination treatment with bisdemethoxycurcumin (40 μM) and potassium iodide achieves a maximum reduction of 3.5 log₁₀ CFU/mL in Candida albicans ATCC 10231 biofilms at 1 hour post-irradiation^[6].
When Bisdemethoxycurcumin (20-80 μM) is used alone, the amount of hydroxyl radicals it generates shows a strong correlation with the reduction degree of Candida albicans ATCC 10231 biofilms; however, when it is used in combination with potassium iodide, the correlation is only moderate after irradiation^[6].

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

Cell Cytotoxicity Assay^[1]

Cell Line:

RAW264.7 murine macrophage cells
Concentration:

2.5, 5, 10, 20, and 40 μM
Incubation Time:

48 h
Result:

Showed no cytotoxicity at 2.5 μM and 5 μM, with cell viability comparable to vehicle control.
Reduced cell viability to ~80% at 10 μM.
Reduced cell viability to ~70% at 20 μM.
Reduced cell viability to ~30% at 40 μM.

Real Time qPCR^[1]

Cell Line:

LPS-stimulated RAW264.7 murine macrophage cells
Concentration:

2.5 μM
Incubation Time:

1 h pre-incubation, followed by 24 h LPS co-incubation
Result:

Significantly reduced LPS-induced elevation of IL-6 mRNA levels.
Significantly reduced LPS-induced elevation of IL-1β mRNA levels.
Significantly reduced LPS-induced elevation of TNF-α mRNA levels.
Significantly reduced LPS-induced elevation of MCP-1 mRNA levels.

Western Blot Analysis^[1]

Cell Line:

LPS-stimulated RAW264.7 murine macrophage cells
Concentration:

2.5 μM
Incubation Time:

1 h pre-incubation, followed by 24 h LPS co-incubation
Result:

Significantly reduced LPS-induced phosphorylation of Akt protein.
Significantly reduced LPS-induced phosphorylation of PI3K protein.
Significantly reduced LPS-induced phosphorylation of p38 protein.
Showed no significant effect on LPS-induced phosphorylation of ERK1/2 or JNK proteins.

Cell Viability Assay^[2]

Cell Line:

ATDC5 chondrocyte cell line
Concentration:

1, 2, 4, 8, 16, 32, 64, 128 and 256 μM
Incubation Time:

24 h; 48 h
Result:

Showed no cytotoxicity at concentrations up to 8 μM after 24 and 48 h.
Significantly reduced cell viability at concentrations ≥16 μM after 24 h.
Significantly reduced cell viability at concentrations ≥16 μM after 48 h.
Exhibited a CC50 value of 14.62 μM in ATDC5 cells after 48 h.

Western Blot Analysis^[2]

Cell Line:

TBHP-stimulated ATDC5 chondrocyte cell line
Concentration:

2, 4, and 8 μM (in combination with 20 ng/mL TBHP)
Incubation Time:

48 h
Result:

Dose-dependently upregulated Collagen II and aggrecan protein expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Dose-dependently downregulated ADAMTS4 and MMP3 protein expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Produced significant changes in protein expression at all tested concentrations compared to TBHP-only treatment.\nDose-dependently upregulated Nrf2 and HO-1 protein expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Dose-dependently downregulated NLRP3, GSDMD, Caspase 1, and IL-1β protein expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Produced significant changes in protein expression at all tested concentrations compared to TBHP-only treatment.

Real Time qPCR^[2]

Cell Line:

TBHP-stimulated ATDC5 chondrocyte cell line
Concentration:

2, 4, and 8 μM (in combination with 20 ng/mL TBHP)
Incubation Time:

48 h
Result:

Dose-dependently upregulated Collagen II and aggrecan mRNA expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Dose-dependently downregulated ADAMTS4, ADAMTS5, MMP3, and MMP9 mRNA expression at 2, 4, and 8 μM compared to TBHP-only treatment.
Produced significant changes in mRNA expression at all tested concentrations compared to TBHP-only treatment.

Immunofluorescence^[2]

Cell Line:

TBHP-stimulated ATDC5 chondrocyte cell line
Concentration:

8 μM (in combination with 20 ng/mL TBHP)
Incubation Time:

24 h
Result:

Significantly reduced ADAMTS5 positive staining area compared to TBHP-only treatment.
Significantly reduced NLRP3 positive staining area compared to TBHP-only treatment.

Cell Autophagy Assay^[3]

Cell Line:

ox-LDL-stimulated mouse aortic vascular smooth muscle cells (VSMCs)
Concentration:

20 μM
Incubation Time:

12 h (pretreated)
Result:

Increased the LC3B-II/LC3B-I ratio, Beclin-1, and ABCA1 protein levels in ox-LDL-stimulated VSMCs.
Decreased p62, PDK1, phosphorylated Akt, and phosphorylated mTOR levels in ox-LDL-stimulated VSMCs, indicating promotion of autophagy via suppression of the PDK1/Akt/mTOR pathway.
Co-treatment with chloroquine reversed BDMC's effects on lipid droplet area, total cholesterol content, triglyceride level, and cholesterol efflux in ox-LDL-stimulated VSMCs, confirming autophagy mediates BDMC's lipid-lowering action.

In Vivo

Bisdemethoxycurcumin (10-40 mg/kg; p.o.; daily; 4 weeks) mitigates atherosclerosis in apoe^−/− mice in a dose-dependent manner, reducing plaque formation, correcting serum lipid profiles, suppressing inflammatory responses, and promoting autophagy via inhibition of the PDK1/Akt/mTOR signaling pathway^[3].
Bisdemethoxycurcumin (100 mg/kg; i.g.; daily; 3 days) alleviates LPS-induced acute lung injury in C57BL/6 mice by activating AMPKα, reducing lung injury, inflammation, and oxidative stress^[4].

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

Animal Model:

apoe−/− (male, 8 weeks of age, fed high-fat diet for 7 weeks to induce atherosclerotic lesions)^[3]
Dosage:

10 mg/kg; 20 mg/kg; 40 mg/kg
Administration:

p.o.; daily; 4 weeks
Result:

Significantly reduced the aortic lumen ratio (plaque diameter/intima thickness) compared to the HFD control.
Reduced serum low-density lipoprotein-cholesterol (LDL-c), total cholesterol, and triglyceride levels, and increased serum high-density lipoprotein-cholesterol (HDL-c) levels (20 mg/kg and 40 mg/kg doses, effects comparable to atorvastatin).
Significantly reduced serum levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α.
Increased protein levels of Beclin-1, ABCA1, and the LC3B-II/LC3B-I ratio in aortic tissue compared to the HFD control.
Decreased protein levels of p62, PDK1, phosphorylated mTOR, and phosphorylated AKT in aortic tissue compared to the HFD control.

Animal Model:

C57BL/6 (8-10-week-old; LPS-induced acute lung injury)^[4]
Dosage:

100 mg/kg
Administration:

i.g.; daily; 3 days
Result:

Significantly reduced LPS-induced lung inflammation score, apoptotic index, LDH activity in lung tissue, lung wet-to-dry ratio, and total protein concentration in BALF.
Decreased airway resistance, increased pulmonary ventilation, and normalized arterial blood gas parameters (PaO₂, PaCO₂, HCO₃^-) in LPS-treated mice.
Suppressed LPS-induced increases in lung and BALF levels of inflammatory cytokines IL-1β, IL-6, and TNF-α, reduced BALF infiltrations of total cells, macrophages, and neutrophils, and inhibited lung MPO activity.
Blocked LPS-elicited phosphorylation and nuclear translocation of NF-κB p65.
Decreased LPS-induced ROS generation and MDA levels in lung tissue, preserved GSH levels, total SOD activity, and SOD2 protein levels, and elevated NRF2 protein levels and transcriptional activity.
Had all protective effects almost completely blunted by AMPKα inhibition with Compound C.

Chemical Information

CAS No. 52328-96-8
Appearance Solid
Molecular Weight 308.33
Formula C₁₉H₁₆O₄
SMILES

O=C(/C=C(O)/C=C/C1=CC=C(O)C=C1)/C=C/C2=CC=C(O)C=C2
Structure Classification
- Ketones, Aldehydes, Acids
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

Handling Instructions (2659 KB)

References

[1]. Wu H, et al. Investigating the Mechanisms of Bisdemethoxycurcumin in Ulcerative Colitis: Network Pharmacology and Experimental Verification. Molecules (Basel, Switzerland). 2022 Dec 21;28(1):68.

[2]. Jin G, et al. Bisdemethoxycurcumin, a curcumin, protects chondrocytes, and reduces cartilage inflammation via the NRF2/HO-1/NLRP3 pathway. Immunity, inflammation and disease. 2024 Feb;12(2):e1195.

[3]. Zuo J, et al. Bisdemethoxycurcumin suppresses the progression of atherosclerosis and VSMC-derived foam cell formation by promoting lipophagy. Naunyn-Schmiedeberg's archives of pharmacology. 2023 Dec;396(12):3659-3670. [Content Brief]

[4]. Li H, et al. Bisdemethoxycurcumin alleviates LPS-induced acute lung injury via activating AMPKα pathway. BMC pharmacology & toxicology. 2023 Nov 20;24(1):63. [Content Brief]

[5]. Hu P, et al. Targeting Liver Fibrosis with Nanoparticle Technology: The Dual-Drug Strategy for Hepatic Stellate Cell Activation Inhibition. ACS applied materials & interfaces. 2025 Apr 30;17(17):25071-25082.

[6]. Damrongrungruang T, et al. Combined bisdemethoxycurcumin and potassium iodide-mediated antimicrobial photodynamic therapy. Heliyon. 2023 Jul;9(7):e17490. [Content Brief]

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1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Bisdemethoxycurcumin

All PI3K Isoforms

All Akt Isoforms

All p38 MAPK Isoforms

All mTOR Isoforms

All AMPK Isoforms

All Interleukin Related Isoforms

All TNF Receptor Isoforms

All NOD-like Receptor (NLR) Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

Bisdemethoxycurcumin Related Classifications

HY-N2942 Related Classifications

Bioz