From Wikipedia, the free encyclopedia
Jump to: navigation, search
Skeletal formula
Enol form
Skeletal formula
Keto form
Ball-and-stick model
Ball-and-stick model
IUPAC name
Other names
Diferuloylmethane; curcumin I; C.I. 75300; Natural Yellow 3
458-37-7 YesY
ChemSpider 839564 YesY
Jmol interactive 3D Image
PubChem 969516
Molar mass 368.39 g·mol−1
Appearance Bright yellow-orange powder
Melting point 183 °C (361 °F; 456 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N verify (what is YesYN ?)
Infobox references

Curcumin (/ˈkərkjuːmən/) is a diarylheptanoid. It is the principal curcuminoid of turmeric, which is a member of the ginger family (Zingiberaceae). It was first discovered about two centuries ago when Vogel and Pelletier reported the isolation of a “yellow coloring-matter” from the rhizomes of Curcuma longa (turmeric) and named it curcumin.[1] Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in organic solvents, while in water the 1,3-diketo dominates.[2]

Curcumin can be used for boron quantification in the curcumin method. It reacts with boric acid to form a red-color compound, rosocyanine.

Curcumin is a bright-yellow color and may be used as a food coloring. As a food additive, its E number is E100.[3]


Adverse effects[edit]

Two preliminary clinical studies in cancer patients consuming high doses of curcumin (up to 8 grams per day for 3-4 months) showed no toxicity,[4] with some subjects reporting mild nausea or diarrhea.[5]


Curcumin incorporates several functional groups. The aromatic ring systems, which are phenols, are connected by two α,β-unsaturated carbonyl groups. The diketones form stable enols and are readily deprotonated to form enolates; the α,β-unsaturated carbonyl group is a good Michael acceptor and undergoes nucleophilic addition. The structure was first identified in 1910 by J. Miłobędzka, Stanisław Kostanecki and Wiktor Lampe.[6]

Curcumin is used as an indicator for boron.[7]


The biosynthetic route of curcumin has proven to be very difficult for researchers to determine. In 1973, Roughly and Whiting proposed two mechanisms for curcumin biosynthesis. The first mechanism involved a chain extension reaction by cinnamic acid and 5 malonyl-CoA molecules that eventually arylized into a curcuminoid. The second mechanism involved two cinnamate units coupled together by malonyl-CoA. Both mechanisms use cinnamic acid as their starting point, which is derived from the amino acid phenylalanine. This is noteworthy because plant biosyntheses employing cinnamic acid as a starting point are rare compared to the more common use of p-coumaric acid.[8] Only a few identified compounds, such as anigorufone and pinosylvin, use cinnamic acid as their starting molecule.[9][10] An experimentally backed route was not presented until 2008. This proposed biosynthetic route follows both the first and second mechanisms suggested by Roughley and Whiting. However, the labeling data supported the first mechanism model in which 5 malonyl-CoA molecules react with cinnamic acid to form curcumin. However, the sequencing in which the functional groups, the alcohol and the methoxy, introduce themselves onto the curcuminoid seems to support more strongly the second proposed mechanism.[8] Therefore, it was concluded the second pathway proposed by Roughly and Whiting was correct.

Curcumin biosynthesis diagram
malonyl-CoA (5)
Biosynthetic pathway of curcumin in Curcuma longa.[8]


In vitro, curcumin has been shown to inhibit certain epigenetic enzymes (the histone deacetylases: HDAC1, HDAC3, and HDAC8) and transcriptional co-activator proteins (the p300 histone acetyltransferase).[11][12][13] Curcumin also inhibits the arachidonate 5-lipoxygenase enzyme in vitro,[14] as well as the enzyme cyclooxygenase.[citation needed]


In Phase I clinical trials, dietary curcumin was shown to exhibit poor bioavailability, exhibited by rapid metabolism, low levels in plasma and tissues, and extensive rapid excretion.[15] Potential factors that limit the bioavailability of curcumin include insolubility in water (more soluble in alkaline solutions) and poor absorption.[15] Numerous approaches to increase curcumin bioavailability have been explored, including the use of absorption factors (such as piperine), liposomes, nanoparticles or a structural analogue.[15]


A survey of the literature shows a number of potential effects under study and that daily consumption over a 3-month period of up to 12 grams were safe.[16] However, several studies of curcumin efficacy and safety revealed poor absorption and low bioavailability.[17]


  1. ^ H. Vogel, J. Pelletier, Curcumin-biological and medicinal properties, Journal de Pharmacie. 1815;I:289.
  2. ^ Manolova, Yana; Deneva, Vera; Antonov, Liudmil; Drakalska, Elena; Momekova, Denitsa; Lambov, Nikolay (2014). "The effect of the water on the curcumin tautomerism: A quantitative approach". Spectrochimica Acta 132A (1): 815–820. Bibcode:2014AcSpA.132..815M. doi:10.1016/j.saa.2014.05.096. 
  3. ^ European Commission. "Food Additives". Retrieved 2014-02-15. 
  4. ^ Cheng, A. L.; Hsu, C. H.; Lin, J. K.; Hsu, M. M.; Ho, Y. F.; Shen, T. S.; Ko, J. Y.; Lin, J. T.; Lin, B. R.; Ming-Shiang, W; Yu, H. S.; Jee, S. H.; Chen, G. S.; Chen, T. M.; Chen, C. A.; Lai, M. K.; Pu, Y. S.; Pan, M. H.; Wang, Y. J.; Tsai, C. C.; Hsieh, C. Y. (2001). "Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions". Anticancer research 21 (4B): 2895–900. PMID 11712783. 
  5. ^ Hsu, C. H.; Cheng, A. L. (2007). "Clinical studies with curcumin". Advances in Experimental Medicine and Biology 595: 471–480. doi:10.1007/978-0-387-46401-5_21. ISBN 978-0-387-46400-8. PMID 17569225. 
  6. ^ Miłobȩdzka, J.; v. Kostanecki, St.; Lampe, V. (1910). "Zur Kenntnis des Curcumins". Berichte der deutschen chemischen Gesellschaft 43 (2): 2163–70. doi:10.1002/cber.191004302168. 
  7. ^ "EPA Method 212.3: Boron (Colorimetric, Curcumin)" (PDF). 
  8. ^ a b c Kita, Tomoko; Imai, Shinsuke; Sawada, Hiroshi; Kumagai, Hidehiko; Seto, Haruo (2008). "The Biosynthetic Pathway of Curcuminoid in Turmeric (Curcuma longa) as Revealed by 13C-Labeled Precursors". Bioscience, Biotechnology, and Biochemistry 72 (7): 1789. doi:10.1271/bbb.80075. 
  9. ^ Schmitt, Bettina; Hölscher, Dirk; Schneider, Bernd (2000). "Variability of phenylpropanoid precursors in the biosynthesis of phenylphenalenones in Anigozanthos preissii". Phytochemistry 53 (3): 331–7. doi:10.1016/S0031-9422(99)00544-0. PMID 10703053. 
  10. ^ Gehlert, R.; Schoeppner, A.; Kindl, H. (1990). "Stilbene Synthase from Seedlings of Pinus sylvestris: Purification and Induction in Response to Fungal Infection" (pdf). Molecular Plant-Microbe Interactions 3 (6): 444–449. doi:10.1094/MPMI-3-444. 
  11. ^ Reuter S, Gupta SC, Park B, Goel A, Aggarwal BB (May 2011). "Epigenetic changes induced by curcumin and other natural compounds". Genes Nutr 6 (2): 93–108. doi:10.1007/s12263-011-0222-1. PMC 3092901. PMID 21516481. Retrieved 12 June 2015. This review summarizes current knowledge about the effect of curcumin on the regulation of histone deacetylases, histone acetyltransferases, DNA methyltransferase I, and miRNAs. ... Because of the differing effect of curcumin on the different subtypes of HDAC enzymes, further research is required to understand the mechanism of curcumin on HDAC expression. ... Thus, curcumin’s ability to suppress p300/CBP HAT activity may be responsible, at least in part, for its potent NF-κB inhibitory activity. 
    Figure 2
  12. ^ Vahid F, Zand H, Nosrat-Mirshekarlou E, Najafi R, Hekmatdoost A (May 2015). "The role dietary of bioactive compounds on the regulation of histone acetylases and deacetylases: a review". Gene 562 (1): 8–15. doi:10.1016/j.gene.2015.02.045. PMID 25701602. 
  13. ^ "Curcumin". IUPHAR. IUPHAR/BPS Guide to PHARMACOLOGY. Retrieved 22 May 2015. 
  14. ^ Bishayee K, Khuda-Bukhsh AR (September 2013). "5-lipoxygenase antagonist therapy: a new approach towards targeted cancer chemotherapy". Acta Biochim. Biophys. Sin. (Shanghai) 45 (9): 709–719. doi:10.1093/abbs/gmt064. PMID 23752617. 
  15. ^ a b c Anand, P.; Kunnumakkara, A. B.; Newman, R. A.; Aggarwal, B. B. (2007). "Bioavailability of curcumin: problems and promises". Molecular Pharmaceutics 4 (6): 807–818. doi:10.1021/mp700113r. PMID 17999464. 
  16. ^ Goel, Ajay; Kunnumakkara, Ajaikumar B.; Aggarwal, Bharat B. (2008). "Curcumin as "Curecumin": From kitchen to clinic". Biochemical Pharmacology 75 (4): 787–809. doi:10.1016/j.bcp.2007.08.016. PMID 17900536. Pilot phase I clinical trials have shown curcumin to be safe even when consumed at a daily dose of 12g for 3 months. 
  17. ^ " Current clinical trials on curcumin". US National Institutes of Health, Clinical Trial Registry. June 2015. 

External links[edit]