Curcumin

Curcumin, a natural compound found in turmeric (a member of the Zingiberaceae family), has been traditionally used as a dye and food preservative. In addition to curcumin, the other two major curcuminoids in turmeric are demethoxycurcumin (D299451, D117978) and bisdemethoxycurcumin (B133654, B423394). All three compounds exhibit antioxidant, anticancer, anti-inflammatory, and antimicrobial activities. Other curcuminoids include 3,4-difluorobenzocurcumin (D276377), which remains in the early stages of research but has demonstrated potential activity across various biological applications, with superior pharmacokinetic bioavailability and stronger pharmacological effects compared to curcumin.

Figure 1. Chemical Structure of Curcumin


1. Curcumin Series Products

Name

ID

Specification/Purity

Curcumin

C400271

Synthetic Origin, Moligand™, ≥98%

Curcumin

C140600

Moligand™, ≥65%

Curcumin

C110685

Analytical Standard, Moligand™

Curcumin

C395975

Moligand™, 0.1% in 95% Ethanol

Curcumin

C477437

Moligand™, Turmeric Powder

Curcumin

C400222

Moligand™, Natural Extract (Isomeric Mixture)

Curcumin

C463317

Moligand™, ≥95%,≥75%(Curcumin), total curcumin content

Curcumin

C408195

Moligand™, 10mM in DMSO


2.Bioactivity Profile of Curcumin

Curcumin exhibits antiviral activity by inhibiting HIV-1 integrase in vitro. HIV integrase is a key regulatory enzyme in the retroviral life cycle. Curcumin also suppresses HIV-1 replication.

Curcumin demonstrates neuroprotective effects, preventing soluble oligomer formation in Aβ-infused animal models, inhibiting new plaque formation, and clearing existing Aβ aggregates, thereby slowing the progression of Alzheimer’s disease.

In breast cancer cell models, curcumin inhibits CXCL1/2 transcription, silences CXCR4 and other pro-metastatic proteins, thereby reducing metastatic potential.

Curcumin may promote the progression of pulmonary lesions from benign hyperplasia to adenomas and carcinoma. This potential carcinogenicity may be associated with modulation of ROS levels and oxidative stress, as well as disruption of p53 conformation, impairing its DNA-binding capacity and cell cycle regulatory function.


References

1. Ferreira VH, Nazli A, Dizzell SE, et al. PLoS One. 2015 Apr 9;10(4):e0124903.

2. Kochi A, Lee HJ, Vithanarachchi SM, et al. Curr Alzheimer Res. 2015;12(5):415-23.

3. Bachmeier B, Mohrenz I, Mirisola V, et al. Carcinogenesis. 2008 Apr;29(4):779-89.

4. Dance-Barnes S, Kock N, Moore J, et al. Carcinogenesis. 2009 Jun;30(6):1016-23.

5. Ali S, Ahmad A, Banerjee S, et al. Cancer Res. 2010 May 1;70(9):3606-17.

 

Aladdin: https://www.aladdinsci.com/

Categories: 技术文章