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Artemisia Anua "Qing Hao" is an herb used in Traditional Chinese Medicine for the treatment of malaria, intestinal worms, febrile diseases, and malignancy. Artemisinin is the active ingredient of Artemisia Anua, and it is one of the most effective treatments so far known against malaria. Artemisinin has also proven to have powerful selective cytotoxic action against cancer cells, and very low to almost non side effect when use appropriately. 

Artemisinin bioavailability and metabolizing rate in the body differs by its derivative forms: Artesunate, Artemether, Dehydroartemisinin, etc., dosage (ratio/body weight), and way of administration. Studies have shown that Artemisinin is poorly absorbed in the gastrointestinal tract, and its oral administration is mainly used against malaria; Artemisinin in small doses is still very effective against malaria. On the other hand, Artemisinin for cancer therapy requires larger doses administered according to body weight and via intramuscular injection, intraperitoneal injection, intratumoral injection, or intravenous infusion. 

Artemisinin treatment protocols for cancer patients require close monitoring with control lab tests and professional clinical supervision; it is typically administered at a health care facility.

In the United States, artemisisin in the form of Artemether is mixed with Lumefantrine (an antibiotic), and it has been approved as a conventional treatment for malaria. Artemisinin/Lumefrantine is not totally artemisinin and it has not known antitumor application.

Dr. Marcelo Lam is one of the physicians more  knowledgeable and experienced on the use of Artemisinin for cancer patients. Dr. Lam's protocols of Artemisnin for oncology application has been adopted by some of the world's leading oncologists. Artemisinin can be provided as a single alternative therapy or as complementary therapy in combination with conventional treatments. 

In China, artemisinin is also available in combination with Gendicine and Oncorine (H101) (gene antineoplastic therapies), Endostar, hyperthermia, HIFU (high intense focused ultrasound ablasion), Kanglaite, and other high tech anticancer therapies.

Artemisinin's strong antitumor actions and low toxicity makes it a suitable anticancer treatment; it is available at our clinic in Miami. Our international medical alliance also facilitate the access to this therapy at state of the art medical facilities in China, and Dominican Republic.     


Review of published data on the use of Artemisinin, and Artemisinin related medicines:


International Journal of Experimental and Clinical Pharmacology
Vol. 82, No. 2, 2008                       

Artemisinin Inhibits Tumor Lymphangiogenesis by Suppression of Vascular Endothelial Growth Factor C, Jun Wanga, Bicheng Zhanga, b, Yan Guoa, Guanghui Lia, Qichao Xiea, Bo Zhua, Jianfei Gaob, Zhengtang Chena. Cancer Institute of People's Liberation Army, Xinqiao Hospital, Third Military Medical University, Chongqing, PR China.

We have previously reported that dihydroartemisinin is found to have a potent ability in influencing lymphatic endothelial cell migration and tube formation. In this study, we investigated the effect of artemisinin on tumor growth, lymphangiogenesis, metastasis and survival in mouse Lewis lung carcinoma (LLC) models. We found that orally administered artemisinin inhibited lymph node and lung metastasis and prolonged survival without retarding tumor growth. Consistent with the decrease in lymph node metastasis, tumor lymphangiogenesis and expression of vascular endothelial growth factor C (VEGF-C) was significantly decreased in artemisinin-treated mice, as compared to control mice. Furthermore, IL-1beta-induced p38 mitogen-activated protein kinase (MAPK) activation and upregulation of VEGF-C mRNA and protein in LLC cells was also suppressed by artemisinin or by the p38 MAPK inhibitor SB-203580, suggesting that p38 MAPK could serve as a mediator of proinflammatory cytokine-induced VEGF-C expression. These data indicate that artemisinin may be useful for the prevention of lymph node metastasis by downregulating VEGF-C and reducing tumor lymphangiogenesis. Copyright 2008 S. Karger AG, Basel.

All cancer cells need plenty of iron to multiply. In other words, cancer cells have a much higher iron concentration than normal cells. During the study, the researchers pumped cancer cells with maximum iron concentrations and then injected artemisinin into them. The results revealed that artemisinin had the properties of killing and inhibiting cancer cells.
(US Patent Document 5,578,637, University of Washington, inventors Dr H.Lai and Dr NP Singh, November 26 1996.) 

In another study, researcher Dr Lai noted even more amazing results involving leukemia cells. He mentioned that the cancer cells were destroyed very quickly within a few hours when exposed to holotransferrin (which binds with transferring receptors to transport iron into cells) and dihydroartemisinin (a more water-soluble form of artemisinin). He further explained that it might be because of the high concentration of iron in the leukemia cells.
(H.Lai and NP Singh, Selective Cancer Cell Cytoxicity from Exposure in Dihydroartemisinin and Holotransferrin, Cancer Letters, 91:41-46, 1995)

This amazing herb was also examined for its activity against 55 cancer cell lines. It was found to be the most active against leukemia and colon cancer and active against melanomas, breast cancer, prostate cancer, CNS and renal cancer. It was also reported that artemisinin's effectiveness was comparable with other standard drugs used to combat cancer. As such, these results and the low toxicity of artemisinin had made this herb to be a potential for cancer chemotherapy.      (Efferth et al, Anti-Malaria Drug is Also active against cancer, Int'l Journal of Oncology, 18;767-773,2001.)

This herb becomes cytotoxic in the presence of ferrous iron. To accommodate a rate of iron intake greater than normal cells, cancer cells surfaces feature greater concentrations of transferrin receptors- cellular pathways that allow iron into a cell. In breast cancer cells, they have 5 to 15 times more transferrin receptors on their surface than normal breast cells. During a recent study, both breast cancer cells as well as normal cells were injected with artemisinin. The results showed that artemisinin effectively killed radiation-resistant breast cancer cells in vitro. However, the effects on the normal breast cells were minimal.This simply goes to show that this herb might be a simple, effective and economical treatment for cancer.    (NP Singh and H Lai, Selective toxicity of dihydroartemisinin and holotransferrin toward human breast cancer cells. Life Sciences, 70:49-56,2001)

When artemisinin was tested on drug sensitive (H69) and multi-drug resistant (H69VP) SCLC cells which were actually injected with transferrin to raise the iron concentration levels, it was found that the cytotoxicity of artemisinin for H69VP cells was ten times lower than for H69 cells. This concluded that artemisinin was part of the drug resistance phenotype. This experiment also indicated that pretreatment of H69 did not lower the iron concentration for artemisinin whereas for H69 VP cells, the iron concentration was lowered to near drug sensitive levels. The researchers therefore concluded that artemisinin could be used together with transferin in drug resistance SCLC.     (Sadava, D et al, Transferrin overcomes drug resistance to artemisinin in human small cell lung carcinoma cells, Cancer Letter, 179,151-156, 2002)

Various studies carried out separately in Germany and Australia, revealed the activities of twenty drugs on leukemia CCRF-CEM cells lines, artemisinin, artesuante, balcalein, baicalin, barberine, bufalin, cantharidin, cephalotaxine, curcumin, daidzein, daidzin, diallyl, disulfide, ginsenoside, Rh2, glycirrhizic acid, isonardosinon, homoharringtonine, nardosinon, nardofuran, puerarin, quercetin, tannic acid and tetrahydronardosinon. The results showed that artesunate increased daunorabicin accumulation in CEM/E1000 cells. As artesunate and bufalin both have abilities to combat leukemia, whether it was applied alone or together with daunonrubicin in multi-resistant cells, these two drugs might be suitable for treating leukemia in the near future.      (Efferth et al, Blood Cells, Molecules, and Diseases 28(2) Mar/April; 160-168, 2002)

Arteminisin could prevent the spread of cancer cells and increase cytotoxicity of perarubicin and doxorubicin in P-glycoprotein-overexpressing, and in MRP- overexpressing, but not in their corresponding drug sensitive cell lines.      (Reungpatthanaphong, P et al Modulation of MDR by Artemisinin, artesunate and DHA in K562, GLC4 Resistant cell lines, Biology Pharmocology Bull. 25(12) 1555-1561, 2002)

When a triterpene and a sesquiterpene were isolated from separation of artemisia stolonifera, both of them proved to be able to destroy cancer cells in non-small cell lung adenocarcinorma, ovarian cancer, skin melanoma, CNS and colon cancer.   (Kwon, Phytochemical constituents of Artemisia stolonifera, Arch.Pharm, Research 24(4):312-315,2001)

When artemisinin's derivative, 9 C-10 was prepared as dimers using novel chemistry, it proved to be able tokill malaria cells. Additionally, dimers 8, 10 and 12 were especially powerful and prevented cancer growth in the NCI in vitro 60 cell line assay.   (Posner, GH et al, Antimalarial, antiproliferative and antitumor activities of Artemisin Derived Dimers, J Medicinal Chemistry, 42(21), 178-181, Oct 1999)

Researchers discovered a novel class of compounds that could destroy cancer cells after modifying artemisinin in one of the experiments conducted recently. This new derivative contained cyano and aryl groups and was very effective in destroying leukemia and human lung carcinoma cells.   (Li, Ying, et al, Novel antitumor artemisinin derivatives targeting G1 phase of the cell cycle, Bioorganic and Medicinal chemistry letters 11:5-8, 2001)

Some artemisinin related endoperoxides that were tested on their abilities to destroy Ehrlich ascites tumor cells (EAT) were proven positive. Surprisingly, its derivatives were even more powerful at destroying cancer cells. This test also confirmed artemisinin and its derivaties abilities to kill EAT cells at higher concentration than those needed for in vitro anti-malaria activities.   (Woerdenbag, HJ et al. Cytotoxicity of artemisinin-related endoperoxides to EATcells, J Natural Products 56(6), 849-856, 1993)

Although artemisinin could not be dissolved in water, it was able to cross the blood brain barrier. It might therefore be useful for curing brain tumors and other brain diseases.

During a recent experiment, an alkaloid of artemisia asiatica was metabolized to small molecules in the digestive tract and was passed through the blood brain barrier. The results showed that it could act as an acetylcholinesterase inhibitor with a blocker of neuroloxicity induced by a beta in human beings that caused AD.   (Heo et al, Inhibitory effects of Artemesia alkaloids on acetylcholine sterase activity from PC12 cells, molecule cells, Jun 30:10(3):253-262)

Clinical Trials On The Use of Artemisinin

In this case, the patient was given artesunate injections and tablets over a period of nine months. His tumor was significantly reduced by about 70 percent just after two months of treatment. The patient also reported that he benefited much from this treatment. It actually prolonged his life and improved his quality of life. Once again, artemisinin had proven its amazing properties in killing cancer cells.  (Singh and Verma, Case report of a laryngeal squamous cell carcinoma treated with artesunate, Archive of Oncology, Vol 10(4), 279-80, 2002)


Investigating if high doses of artemisinin could produce neurotixicity such as ding gait disturbances, loss of spinal and pain response, respiratory depression and ultimately cardiopulmonary arrest in large animals.

When artemisinin was given to monkey at 292 mg/kg over 1 to 3 months, they showed no toxicity.   (Journal of Traditional Chinese Medicine 2(1) : 31-36, 1982) 

In pharmacokinetic studies, 250 mg tablets of artemisin and artesunate tablets were used. Both forms of tablets were well tolerated and there were no negative side effects.    (Benakis et al. Pharmacokinetics of artemisinin and artesunate after oral administration in healthy volunteers. American Journal of Tropical Medicine Hyg, Jan;56(1): 17-23, 1997)

During a study, healthy volunteers were given 250 mg of tablets of artemisinin and artesunate orally. Thee researchers reported that in the case of Artemisinin, the mean maximun drug concentration C= 0.36 microgram/ml, appearance half life T-0.62 hr,  distribution hal life t(12) a= 2.61 hr, decline half life t(12) = 4.34 hr, total area under concentration curve (AUC) =1.10 microgram hg/ml its main metabolite, dihydroartemisinin was measured in plasma.  On the other hand, half lives were more shorter in the case of artesunate (a syntetic form of the drug). (Benakis, et al, Dept of Pharmacology, Geneva U Swiss, Am J Trop Med Hyg, Jan; 56(1): 17-23, 1997.   
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