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  • Brand : BIOFRON

  • Catalogue Number : BF-D3011

  • Specification : 98%

  • CAS number : 71939-50-9

  • Formula : C15H24O5

  • Molecular Weight : 284.35

  • PUBCHEM ID : 3000518

  • Volume : 100mg

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Catalogue Number


Analysis Method






Molecular Weight



White needle crystal

Botanical Source

Artemisia annua

Structure Type



Standards;Natural Pytochemical;API




Dihydroartemisinin/Dihydroartemisin/3,12-Epoxy-12H-pyrano[4,3-j]-1,2-benzodioxepin-10-ol, decahydro-3,6,9-trimethyl-, (3R,5aS,6R,8aS,9R,10S,12R,12aR)-/Cotecxin/Dihydroginghaosu/(1S,4S,7R,8S,11R,12S,13R)-1,7,11-Trimethyl-3,5,14,15-tetraoxatetracyclo[]hexadecan-6-ol/(1R,4S,5R,8S,9R,10S,12R,13R)-1,5,9-Trimethyl-11,14,15,16-tetraoxatetracyclo[]hexadecan-10-ol/Alaxin/[3H]-(10R/S)-Artenimol/Salaxin/artenimol/3,12-Epoxy-12H-pyrano(4,3-j)-1,2-benzodioxepin-10-ol, decahydro-3,6,9-trimethyl-, (3R,5aS,6R,8aS,9R,10S,12R,12aR)-/(3R,5aS,6R,8aS,9R,12S,12aR)-decahydro-3,6,9-trimethyl-3,12-epoxy-12H-pyrano[4,3-j]-1,2-benzodioxepin-10-ol/(3R,5aS,6R,8aS,9R,12R,12aR)-decahydro-3,6,9-trimethyl-3,12-epoxy-12H-pyrano[4,3-j]-1,2-benzodioxepin-10-ol/dihyhydroartemisinin/DHQHS 2/(5aS,6R,8aS,9R,10S,12R,12aR)-3,6,9-trimethyldecahydro-3,12-epoxy[1,2]dioxepino[4,3-i]isochromen-10-ol/3,12-Methano-5aH,7H-1,2,5-trioxepino[3,4-j][2]benzopyran-7-ol, octahydro-3,8,11-trimethyl-, (3S,5aS,8R,8aS,11R,12S,12aR)-/Dihydroarteminisin/dihydroquinghaosu/(3R,5aS,6R,8aS,9R,10S,12R,12aR)-3,6,9-trimethyldecahydro-3,12-epoxy[1,2]dioxepino[4,3-i]isochromen-10-ol/Cotexin/Dihydroqinghaosu




1.3±0.1 g/cm3



Flash Point

181.0±27.9 °C

Boiling Point

375.6±42.0 °C at 760 mmHg

Melting Point



InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:71939-50-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Tuberculosis is one of the leading causes of mortality worldwide. Resistance against the frontline anti-tubercular drugs has worsened the already alarming situation, which requires intensive drug discovery to develop new, more effective, affordable and accessible anti-tubercular agents possessing novel modes of action.

Chemical transformation of dihydroartemisinin for anti-tubercular lead optimization.

Dihydroartemisinin, a metabolite of artemisinin was chemically converted into eight acyl derivatives and were evaluated for anti-tubercular potential against H37Rv virulent strain of Mycobacterium tuberculosis by agar-based proportion assay. Further, synergistic activity of 12-O-m-anisoyl dihydroartemisinin was also studied with the front-line anti-TB drugs, isoniazid and rifampicin.

The results showed that all the derivatives were active but out of eight, 12-O-m-anisoyl dihydroartemisinin and 12-O-p-anisoyl dihydroartemisinin were significantly active (MIC 25.0 µg/mL). In synergistic activity evaluation, the 12-O-m-anisoyl dihydroartemisinin derivative showed reduction in MIC (by 1/8th, i.e. 3.12 µg/mL and that of rifampicin by ¼th, i.e. 0.05 µg/mL) with the front-line anti-TB drug, rifampicin. The sumfractional inhibitory concentration (Σ FIC) was 0.375.

These results suggested a synergistic effect of the 12-O-m-anisoyl dihydroartemisinin with rifampicin and established its base for the development of anti-tubercular agents from an in-expensive and non-toxic natural product. To the best of our knowledge this is the first ever report on the anti-tubercular potential of dihydroartemisinin and its derivatives.

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.


Anti-tubercular activity; Dihydroartemisinin; Semi-synthetic derivatives; Synergistic effect Artemisia annua; Tuberculosis.


Dihydroartemisinin and its Analogs: A New Class of Antitubercular Agents.


Kalani K1, Chaturvedi V2, Trivedi P2, Tondon S3, Srivastava SK1.

Publish date





The present study aimed to investigate the effect of dihydroartemisinin on the proliferation of chemotherapy‑resistant C6 rat glioma cells. The results revealed that incubation of C6 glioma cells with a range of dihydroartemisinin concentrations for 48 h led to a significant (P<0.02) reduction in the cell number. There was a ‑0.8-fold reduction in the cell count following treatment with 20 µM dihydroartemisinin when compared with the control cultures. Analysis of DNA synthesis using bromodeoxyuridine (BrdU) staining demonstrated a reduction in the BrdU‑labeling index (LI) following treatment with 20 µM dihydroartemisinin. There was a 6‑fold reduction in the BrdU‑LI compared with the control cultures. Incubation of the C6 glioma cells with dihydroartemisinin led to a concentration dependent reduction in the level of cyclic adenosine 3′,5’‑monophosphate following 48 h. The percentage of apoptotic cells in the cultures incubated with 20 µM dihydroartemisinin was 54.78% compared with 2.57% in the control cultures. Incubation of the C6 glioma cells with dihydroartemisinin for 48 h led to a reduction in the percentage of cells in G2/M phase with an increase in G0/G1 phase. The control cells exhibited spindle‑shaped morphology and were actively undergoing mitosis following 48 h of culture. The morphological characteristics of the cells treated with dihydroartemisinin were demonstrated to be round with small surface projections. Therefore, treatment of glioma cells with dihydroartemisinin exhibited an antitumor effect by the induction of apoptosis. Therefore, dihydroartemisinin should be evaluated further in the animal models for the treatment of glioma.


Dihydroartemisinin treatment exhibits antitumor effects in glioma cells through induction of apoptosis.


Xu CH1, Liu Y1, Xiao LM1, Guo CG1, Zheng SY1, Zeng EM1, Li DH1.

Publish date

2017 Dec




To investigate the effects of dihydroartemis (DHA) on influenza A virus (IAV) A/PR/8/34 (H1N1) induces the pro-inflammatory factor and protein of extracellular signal regulated kinase (ERK) signaling pathway expression in bronchial epithelial cells.

The BEAS-2B cells were treated with different concentrations of DHA (i.e.,0, 12.5, 25,50 and 100 μmol/L) for 24 h and the effect of DHA on the viability of BEAS-2B cells were measure by CCK8 method. The BEAS-2B cells were absorbed with IAV for 1 h, and then were treated with different concentrations of DHA (i.e., 12.5, 25 and 50 μmol/L) for 24 h, meanwhile, the normal control group and IAV group were established. The mRNA and protein expression levels of tumor necrosis factor-α (TNF-α) and interleukin (IL-6) were measured by real time quantitative PCR (RT-qPCR) and enzyme linked immunosorbent assay (ELISA), the expression levels of phospho-ERK (p-ERK) proteins were tested by Western blot (WB). Then, an ERK agonist (20 ng/mL) was used to treat BEAS-2B cells (the groups were divided into normal control group, DHA group, DHA+IAV group, ERK agonist group and DHA+IAV+ERK agonist group) for 24 h, and to observe the effect of DHA on inhibiting IAV induce the TNF-α, IL-6 and p-ERK expression in the BEAS-2B cells.

The BEAS-2B cells viability was not significantly different from that of the normal control group after treatment with DHA (i.e., 12.5, 25, and 50 μmol/L). The expression levels of TNF-α, IL-6 mRNA and TNF-α, IL-6, p-ERK protein in IAV group were significantly up-regulated compared with that in the normal control group ( P<0.05), meanwhile, compared with the IAV group, the expression levels of TNF-α, IL-6 mRNA and TNF-α, IL-6, p-ERK protein showed dose-dependent decrease in IAV+DHA group ( P<0.05). However, ERK agonists attenuated the DHA inhibit IAV induced the proinflammatory factors TNF-α, IL-6 secretion and the p-ERK protein expression of ERK signaling pathway in BEAS-2B cells.

These data suggest that DHA can inhibit IAV induces the TNF-α and IL-6 expression in BEAS-2B cells through ERK signaling pathway.

Copyright© by Editorial Board of Journal of Sichuan University (Medical Science Edition).


Dihydroartemis; ERK signaling pathway; Influenza A virus H1N1


[The Effects and Mechanisms of Dihydroartemisinin on Influenza A Virus H1N1 Induces TNF-α and IL-6 Expression in Bronchial Epithelial Cells].


Ou L1, Qin K1, Yang ZX2, Bie MJ3,4.

Publish date

2020 Mar

Description :

Dihydroartemisinin is a potent anti-malaria agent.