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About Dr. Zhang

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Formula List
AI # 3 Capsule
Allicin Capsule
Artemisia Capsule
Artemisia 2 Capsule
(Double Potency)
BM Capsule
Capillaris Combination
Circulation P Capsule
Copmine Formula
Coptis Capsule
Cordyceps Capsule
DH-Artemisinin Capsule
Gall Formula 1
Gineseng and Atractylodes Formula
Glycyrrhizin Capsule
Hepa Formula 1A
Hepa Formula 2
HerbSom Capsule
HerbZac Capsule
HH Tablets
HH 2 Capsule
(Double Potency)
Ligustrin Capsule
Milk Thistle Plus
MVM Formula
Olivessence Capsule
Puerarin Capsule
R-5081 Capsule
R-OBG Capsule
Schisandra Plus
TGP formula
Yunan Paiyao Capsule
DH-Artemisinin Capsule
Recommended Daily Dose:
1 Capsules, 3 times a Day

(Individual Dosage May Vary. Please Consult Health Care Professional)

Dihydroartemisinin (DHA) has been used as the 1st line anti-malaria remedy by the World Health Organization. Its application has been expanded to treating the malaria-like protozoa infection, babesiosis.  In addition to its anti-malaira and anti-protozoa actions, DH-Artemisinin can also be used as a supportive treatment agent in autoimmune and cancer related disorders.

1. Original Plant: Traditional Chinese medicinal herb Qing Hao (Herba Artemisiae annuae), a sweet wormwood plant.

2. Chemical Composition:

DHA is a molecularly modified derivertive of artemisinin. It is extracted and purified from Herba Artemisiae annuae. It is a sesquiterpene lactone with the molecular formula C15H24O5 and molecular weight: 284.3. DHA is the metabolite of artemisinin and its derivertives include artemisinin, artemether, artesunate, and DHA in the body. It is the pharmacodynamic molecule equivalent of these derivertives.

3. Pharmacology:

A.      Anti-Malaria Effects:

DHA possesses strong anti-malarial actions and is lethal to the malaria protozoa Endoerythrocytic plasmodium. Compared to chloroquine, symptomatic control and negative plasmodium conversion were achieved more rapidly using DHA. In addition, compared to chloroquine, resistance to DHA by plasmodia developed at a much slower rate. It is also effective against chloroquine-resistant strains. Alteration of the molecular structure of artemisinin to DHA has reduced relapse rates. (UNDP 1984, Jian QB et al. 1982, Guan WJ et al., 1986, Xuan WJ et al., 1990, Yie B et al., 1991, Eillis et al., 1985, Smithuis F. et al.,2006). Under the electron microscope, it was discovered that DHA actions mainly affect the membranous structures of the intra erythrocyte asexual plasmodium, primarily on the food vacuole membrane, surface membrane, and mitochondrial membrane. Secondarily, its mechanisms also affect the nuclear membrane, endoplasmic reticulum and intra-nuclear chromosomes. The alteration of the food vacuole membrane interrupts the nutrition intake abilities of the plasmodium. Following the deprivation of amino acids, auto-phagocytic vacuoles were found to continually excrete out of the protozoa, resulting in the loss of large amounts of cytoplasm leading to the destruction of the internal structures and cell death. (Jaing et al., 1986, Li et al., 1983, Qinghao Research Group, 1982, Yie ZG et al., 1986, Chen DJ et al., 1980).


B.      Anti-Babesia Effects:

The application of DHA in treating babesiosis was based on the similarities between babesiosis and malaria. Conventional medicine also uses anti-malarial therapies to treat babesiosis. From clinical observations, it was found that this substance was able to trigger the Herxheimer’s reaction and release typical babesiosis symptoms. Moreover, compared with conventional treatment, it has shown fewer side effects and requires a shorter treatment course.

C.      Anti-Cancer Effects:

DHA can induce cancer cell death through apoptosis in a dose- and time-dependent manner via caspase-3-dependent mitochondrial death pathway observed in ASTC-a-1 cells of lung cancer. It has been studied as a possible anticancer drug in the clinical treatment of lung adenocarcinoma (Lu, YY et al., 2009). DHA at a concentration of 5-25 μM inhibited the growth and induced apoptosis of C6 cells in a concentration- and time-dependent manner; however, it was much less toxic to rat primary astrocytes. In this concentration range, it also increased the generation of reactive oxygen species in C6 cells. These effects of DHA were enhanced by ferrous ions and reduced by the iron chelator deferoxamine (Huang XJ et al., 2007).
DHA also demonstrated the ability to promote cancer cells to enter apoptosis. Singh NP et al. reported that in cancer cell line Molt-4 cells cultured in a medium containing 200 microM of DHA, it was found that DHA treatment significantly decreased cell counts and increased the proportion of apoptosis compared to the control groups. No necrotic cells were observed. From this study, it was concluded that the rapid induction of apoptosis in cancer cells after treatment with DHA indicates that it may be an effective anti-cancer agent (Singh Np et al., 2004, Schaller, 2006).

Another derivative of artemisinin, deoxyartemisitene, has been tested to have suppressive actions on 14 different types of human cancer cell lines. (Galal AM, et al., 2002) The following cancers were shown to have the highest sensitivity to the substance: leukemia, colon cancer, and melanoma. (Berger TG et al., 2005, Efferth T, et al., 2002) It has also shown suppressive effects on following cancer types: breast cancer, ovarian cancer, prostate cancer, brain cancer, and kidney cancer. (Efferth T, et al., 2006, Anfosso L, et al., 2006, Paik IH, et al., 2006, Galal AM, et al., 2002, Lai H, et al., 2005, Lee CH, et al., 2000, Singh NP, et al., 2001) A similar anti-cancer action was found in DHA (Singh NP, et al., 2001). It selectively affects cancer cells without harming normal cells, and contains a wide anti-cancer spectrum. DHA can be used immediately after the initial cancer diagnosis to prepare the patient for oncology therapies. It can also be used as a tertiary preventive measure following surgery, chemotherapy, or radiation treatments to prevent relapse and metastasis.


D.      Immune-regulatory effects:

Serum interferon level increased and maintained at the elevated level for 24 hours in mice who were given DHA. Increased phagocytosis started 24 hours after administration and stayed elevated for 72 hours. It increased the percentage of phagocytosis of phagocytes and increased phagocytic index. The elevated phagocytic activity may be a result of the effects of interferon. It can reduce serum IgG in sensitized animals and increase the weight of the spleen. It has obvious suppressive effects on humoral and cellular immunity in mice and can reduce the amount of antibody producting cells and also suppress delayed allergic reactions, as well as suppress IL-2 production in mice spleen. These effects explain its usage in treating systematic lupus erythematosus (SLE). (Shen M et al., 1983, Zhang D et al., 1989, Chen H et al., 1988, Qien RS et al., 1981, Zhao KC et al., 1988)

4. Pharmacokinectics:

Studies have found that DHA is widely dispersed and rapidly absorbed, metabolized, and excreted. There was no evidence of toxic accumulation after long-term use. (Chen S et al., 1980, Zhu DY et al., 1980, 1983, Research Group on Qinghaosu 1982, Ning DX et al., 1987). When used in the recommended dosage orally, no toxic side effects were reported. (Gordi, T, 2004)

5. Clinical Applications

A.      Malaria: A 100% cure rate was achieved in large number cases of tertian malaria and subtertian malaria. DHA is one of the best treatments for multidrug-resistant Plasmodium falciparum malaria and is well tolerated by all age groups.

B.      Babesiosis: In our clinic, the treatment course is approximately 90 days. Most patients see the babesiosis test turn negative after one course. Some patients require a second course of treatment.

C.      SLE and lupus erythematosus discoides: Almost every case experienced remission in varying degrees. During the beginning of treatment, symptoms may temporarily worsen then gradually improve. (Zhuang GK et al., 1979)

D.      Adjunctive treatment for cancer patients for primary and tertiary prevention of relapse and metatasis.

6. Dosage: Each capsule contains 40 mg of DHA, take one capsule three times a day. (Total daily dose is 120mg *)

(*For treating malaria, the daily recommended dose is 60 mg)

7. References:

Anfosso L., et al., Microarray expression profiles of angionenesis-related genes predict tumor cell response to artemisinins. Pharmacogenomics J. 6:269-78, 2006

Berger TG, et al., Artesunate in the treatment of metastatic uveal melanoma – first experiences, Oncol Rep. 2005; 14:1599-603

Chen DJ et al., Chinese Medical Journal, 1980,60(7):422

Chen H et al., Academic Journal of Penbu Medical College, 1988, 13(3):195

Chen S et al., Journal of New Chinese Medicine, 1980 (1):37

Efferth T, Olbrich A, Bauer R: mRNA expression profiles for the response of human tumor cell lines to the antimalarial drugs artesunate, arteether, and artemether. Biochem Pharmacol 64:617-623, 2002.

Efferth T., et al., Molecular pharmacology and pharmcogenomics of artemisinin and its derivatives in cancer cells. Curr Drug Targets, 7:407-21, 2006

Eillis et al., Ann Troo Med Parasito, 1985, 79(4):367

Galal AM, et al., Deoxyartemisinin derivatives from photooxygenation of anhydrodeoxydihydroartemisinin and their cytotoxic evaluation. J. Nat Prod. 65:184-8, 2002

Gordi T, Lepist EI: Artemisinin derivatives: toxic for laboratory animals, safe for humans? Toxicol Lett 2004, 147:99-107.

Guan WJ et al., Academe Journal of Second Military Medical University, 1986, 7(2):123

Huang XJ et al., Dihydroartemisinin exerts cytotoxic effects and inhibits hypoxia inducible factor-1α activation in C6 glioma cells, J. Pharmacy &Pharmacology, 2007, 59 (6):849-85

Jian QB et al., The lancet, 1982, 8(7):285

Jiang et al., Foreign Medicine, Chinese Medicine, 1986, 8(2):54

Lai H, Singh NP: Selective cancer cell cytotoxicity from exposure to dihydroartemisinin and holotransferrin. Cancer Lett 91:41-46, 1995.

Lai, H., et al., Effects of artemisinin-tagged holotransferrin on cancer cells. Life Sciences, 2005 (Vol. 76) (No. 11) 1267-1279

Lee CH, Hong H, Shin J, et al.: NMR studies on novel antitumor drug candidates, deoxoartemisinin and carboxypropyldeoxoartemisinin. Biochem Biophys Res Comm 274:359-369, 2000.

Li et al., Trans Roy Soc Trop Med Hyg, 1983, 77(4):522

Lu, YY et al., Dihydroartemisinin (DHA) induces caspase-3-dependent apoptosis in human lung adenocarcinoma ASTC-a-1 cells, Journal of Biomedical Science 2009, 16:16

Ning DX et al., Chin J of Pharmacology and Toxicology, 1987, 1(2):135

Paik IH, et al., Second generation, orally active, antimalaria, artemisinin-dereved troxane dimmers with high stability, efficacy and anticancer activity. J. Med. Chem, 49:2731-4, 2006

Qien RS et al., Journal of Traditional Chinese Medicine, 1981, 6:63

Qinghao Research Group, Journal of Traditional Chinese Medicine, 1982, 2(1):17

Research Group on Qinghaosu and Its Derivatives as Antimalarials, J Trad Chin Med, 1982,2(1):25

Schaller J., Artemisinin, Artesunate, Artemisinic Acid and Other Derivatives of Artemisia Used for Malaria, Babesia and Cancer, Hope Academic Press, Tampa, Florida, 2006, p.55

Shen M et al., Chinese Science B, 1983, 10:928

Singh NP, et al., Artemisinin induces apoptosis in human cancer cells. Anticancer Res. 24: 2277-80, 2004

Singh NP, Lai H: Selective toxicity of dihydroartemisinin and holotransferrin toward human breast cancer cells. Life Sci 70:49-56, 2001

Smithuis F. et al., Efficacy and effectiveness of dihydroartemisinin-piperaquine versus artesunate-mefloquine in falciparum malaria: an open-label randomised comparison, 2006, The Lancet, 367(9528): 2075 - 2085,

UNDP/World Bank/WHO. TDR/CHEMALSWG (4)/(QHS)/ 1981:3)

Xuan WJ et al., Academic Journal of Materia Medica (Chinese),1990, 25(3):220

Yie B et al., Academic Journal of Materia Medica (Chinese),1991, 26(3):228

Yie ZG et al., Journal of Parasite and Parasitic Diseases, 1986, 4(4):260

Zhang D et al., Chinese Pharmacology Bulletin, 1989, 5(1):37

Zhao KC et al., Academic Journal of Materia Medica (Chinese),1988, 21(10):736

Zhu DY et al., Academic Journal of Materia Medica (Chinese),1980, 15(8):509

Zhu DY et al., Chinese Academic Journal of Pharmacology, 1983, 4(3):194

Zhuang GK et al., Journal of New Chinese Medicine, 1979 (6):39