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Old 01-01-2010, 05:57 PM   #1
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Artemisinin (anti-malarial, anti-cancer)

(Anti Il-8/CSC, C-myc, PI3k/Akt, DR5, mmp/invasion, Anti ER, crosses BBB, creates resistance to Doxo?, w/Cyclo, w/Vin, w/Cis, protocols, toxicities)


How does Artemisinin kill cancer cells?
- Cancer cells need iron to enable them to grow aggressively, hence cancer cells typically absorb a significantly larger amount of iron than normal, healthy cells. When Artemisinin comes in contact with these irons in the cancer cells, it would trigger a chemical reaction and form charged atoms that chemists call "free radicals". The free radicals attack the cancer cell membranes, breaking them apart and killing them. This is why Artemisinin is highly toxic to cancer cells. Tests have been conducted to show that Artemisinin causes rapid and extensive damage and death in cancer cells and yet has relatively low toxicity to normal cells.
UW scientists report success in herb enhanced to fight cancer
Drug now used against malaria

The herb, artemisinin, or sweet wormwood, is an ancient Chinese medicinal herb already commonly used to treat malaria worldwide. Because its effect in the body is relatively brief, it is often used in a pharmaceutical combination with other routine anti-malarial drugs -- an approach known as ACT, artemisinin-based combination therapy.

"The connection here is iron," explained Sasaki.
Artemisinin is good at killing malaria parasites because it reacts and becomes highly toxic in the presence of iron, he said. Malaria parasites cause illness in humans by consuming red blood cells, which contain iron in the hemoglobin protein that carries oxygen in the blood. Similarly, cancer cells use lots of iron as they proliferate in tumors.
Recognizing this connection, Lai and Singh in the 1990s began exploring the possibility of using this Chinese herb as a cancer drug. They continued to publish about it, and the UW patented the idea. Sasaki joined the team in 2000, and the scientists formed a local company, Artemisia Biomedical Inc., to explore how to turn this into a commercial drug therapy.

Recognizing this connection, Lai and Singh in the 1990s began exploring the possibility of using this Chinese herb as a cancer drug. They continued to publish about it, and the UW patented the idea. Sasaki joined the team in 2000, and the scientists formed a local company, Artemisia Biomedical Inc., to explore how to turn this into a commercial drug therapy. In the report published this month, the UW trio describe how they have created their own kind of artemisinin compound to enhance the herb's cancer-killing abilities. Basically, the scientists manipulated the herb's protein surface and boosted it with iron. When the cancer cells consume the compound, it releases toxic chemicals that kill the cells.
"The compound is like a little bomb-carrying monkey riding on the back of a Trojan horse," Lai said in a statement accompanying the report. Lai, who is perhaps best known publicly for his controversial studies linking cancer and cell phone use, is not afraid to mix humor with science, let alone metaphors.
Most chemotherapy drugs today have serious side effects, Sasaki said, because they generally kill one healthy cell for every 10 cancer cells. The UW's artemisinin compound used in cell cultures and in rats with breast cancer showed much better targeting and less collateral damage -- killing about 12,000 cancer cells for every healthy cell killed. Even regular artemisinin, without the UW alteration, only kills one good cell for every 100 cancer cells, he said.

[The article discusses risk concerns of the new (patented) more potent formulation/combination because it contains iron to boost the effects of Artemisinin. It doesn't seem to specifically caution against using Artemisinin by itself without iron supplementation.]

Mechanism of action according to Artemesia: LINK

Artemisinin in Cancer treatment-slide presentation:

Dr. Narendra P. Singh, UW-Seattle


•Artemisinin is a sesquiterpene lactone isolated from the plant Artemesia annuaL. (has been used for the treatment of malaria).
•Dr.Zhenxing Wei was first to isolate artemisinin in 1970.•The artemisinin molecule contains an endoperoxide bridge that reacts with a ferrous iron to form free radicals
•There are several analogs of artemisinin including artesunate and artemether.

How does Artemisinin work?
•Artemisinin causes the cancer cell to commit suicide.
•The artemisinin molecule contains an endoperoxide bridge that reacts with a ferrous iron atom to form free radicals
•Generation of free radicals leads to macromolecular damages and cell death.
•Cancer cells have a very high iron uptake and thus they are more susceptible.
Research on Artemisinin:
Breast Cancer Cells in vitro undergo rapid and almost complete cell death (98%) after treatment with dihydro-artemisinin and holotransferrin.
Breast cancer cells were completely non-viable after 8 hours of treatment with holotransferrinand dihydroartemisinin, as proved by replating. Normal breast cell counts slightly decreased with the same treatment, suggesting some damage to cells.

•Dog trials were begun soon after encouraging results in MOLT-4 experiments (1994-1995).
•Dogs of different breeds (male and female) having various types of cancers (lymphosarcoma, breast adenocarcinoma, osteosarcoma, ETC) were treated.
•Results: Specific results varied with dogs, but generally positive. Tumor sizes were drastically reduced. No reoccurrence of cancer in 5 dogs operated and given artemisinin.

Frequently Asked Questions
•Q. Do we need Holotransferrin?
•A. No we do not need Holotransferrin. Enough iron can be found in our daily diet.
•Q. What form of iron works with artemisinin?
•A. Artemisinin reacts with ferrous iron (Fe2+). Transferrin carries ferric iron (Fe3+) to the cell surface, the ferric iron is then converted to the ferrous form (Vitamin C can do this) and reacts with artemisinin
•Q. Should an iron supplement be taken along with artemisinin?
•A. No. This is not necessary. Iron is abundant in our diet in two forms: heme iron (found in animal products) and non-heme iron (found in plant products). Vitamin C helps in the absorption of non-heme iron, which is generally harder to absorb.
•Q. Is a combination of Artemisinin derivatives better?
•A. A mixture of artemisinin, artesunate and artemetherand is slightly better than individual components.
•Q. How does Vitamin C affect the results?
•A. If taken after breakfast and after lunch, it enhances the iron absorption from the stomach. Iron is taken up more by cancer cells and thus Vitamin C makes cancer cells more susceptible for killing by artemisinin.
•Q. How do other vitamins and antioxidants affect the results?
•A. Different studies show different results with vitamin E. Our own work shows glutathione enhances cancer cell growth and reduces the efficacy of artemisinin.
•Q. What are toxic effects?
•A. In general, artemisinin and its analogs are relatively safe drugs with no obvious adverse reactions or noticeable side effects. Some patients complain of skin irritation and scratching in 1 to 2mg/kg/day doses.
•Anemia and weakness is reported by several patients on artemether but not by those on artesunate and artemisinin. Artemisinin does not have affinity to normal RBC unlike artemether.
•Q. Are there some on going clinical trial.
•A. No official clinical trial, but Dr. Joy Craddick MD (joyhealth@earthlink.net) and Dr. Dwight McKee MD (dmckeemd@aol.com) are conducting a clinical trial started 3 months ago on 30 cancer patients in Portland area. FDA approved a canine trial in DC area.

Wormwood (Artemsisia Annua) contains Artemisinin: a Natural Remedy for Breast Cancer


Scientists in Seattle[1] [2] have shown that a compound called Artemisinin, extracted from the Wormwood plant (Artemsisia Annua L.), seeks out and destroys breast cancer cells, leaving healthy cells unharmed.

Since cancer is characterised by out-of-control cell division, cancer cells have much higher iron concentrations than do normal cells. On their surfaces, cancer cells also have more so-called transferrin receptors, cellular pathways that allow iron to enter than healthy cells. In the case of breast cancer, the cells have five to 15 times more transferrin receptors on their surface than normal breast cells. About seven years ago Henry Lai reasoned, why not target cancer cells with the anti-Malaria treatment?

Scientists in Seattle[1] [2] have shown that a compound called Artemisinin, extracted from the Wormwood plant (Artemsisia Annua L.), seeks out and destroys breast cancer cells, leaving healthy cells unharmed.

The patented version:
The thrust of the strategy, according to Henry Lai, is to pump up cancer cells with even more iron and then introduce Artemisinin to selectively kill them. A compound known as Holotransferrin which binds with transferrin receptors transports iron into cells and further increases the cells' iron concentrations.

Cells exposed to just one of the compounds showed no appreciable effect, Henry Lai reports. But the response by cancer cells when hit with first Holotransferrin, then Artemisinin, was dramatic.
[Not sure what the single, ineffectual compound that had "no appreciable effect" was. The below all suggests Artemisinin by itself has effect.]

Artemisinin and Cancer


[QUOTE]Some seven years ago, Dr. Lai, aware of the high accumulation of iron in cancer cells, wondered if this same mechanism might work in cancer cells, wondered if this same mechanism might work in cancer treatment. He and his colleague, Dr. Singh, conducted experiments in laboratory cancer cells documenting a 100% kill rate of breast-cancer cells in just hours. More importantly, it left normal breast cells and white blood cells unscathed.
Then, one year ago, an article appeared in a major cancer journal demonstrating significant artemisinin anticancer activity in a wide variety of laboratory cultured cancer cells. But astonishingly, cancer’s resistance to common chemotherapy drugs shows no such resistance to artemisinin. It does not have the chemical structure a cancer cell requires to develop resistance! (This was reported recently in the International Journal of Oncology 18; 767-773, 2001 by Efferth, et al.) [QUOTE]

May conflict with Doxorubicin (Adriamycin)??

Br J Pharmacol. 2009 Apr;156(7):1054-66. Epub 2009 Mar 9.
Artemisinin induces doxorubicin resistance in human colon cancer cells via calcium-dependent activation of HIF-1alpha and P-glycoprotein overexpression.

Riganti C, Doublier S, Viarisio D, Miraglia E, Pescarmona G, Ghigo D, Bosia A.
Department of Genetics, Biology and Biochemistry, University of Torino, and Research Center on Experimental Medicine (CeRMS), Via Santena, Torino, Italy. chiara.riganti@unito.it
BACKGROUND AND PURPOSE: Artemisinin is an antimalarial drug exerting pleiotropic effects, such as the inhibition of the transcription factor nuclear factor-kappa B and of the sarcoplasmic/endoplasmic reticulum Ca(++)-ATPase (SERCA) of P. falciparum. As the sesquiterpene lactone thapsigargin, a known inhibitor of mammalian SERCA, enhances the expression of P-glycoprotein (Pgp) by increasing the intracellular Ca(++) ([Ca(++)](i)) level, we investigated whether artemisinin and its structural homologue parthenolide could inhibit SERCA in human colon carcinoma HT29 cells and induce a resistance to doxorubicin. EXPERIMENTAL APPROACH: HT29 cells were incubated with artemisinin or parthenolide and assessed for SERCA activity, [Ca(++)](i) levels, Pgp expression, doxorubicin accumulation and toxicity, and translocation of the hypoxia-inducible factor, HIF-1alpha. KEY RESULTS: Artemisinin and parthenolide, like the specific SERCA inhibitors thapsigargin and cyclopiazonic acid, reduced the activity of SERCA. They also increased intracellular calcium concentration ([Ca(++)](i)) and Pgp expression and decreased doxorubicin accumulation and cytotoxicity. The intracellular Ca(++) chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, and the inhibitor of calmodulin-dependent kinase II (CaMKII) KN93 prevented these effects. CaMKII is known to promote the phosphorylation and the activation of HIF-1alpha, which may induce Pgp. In HT29 cells, artemisinin and parthenolide induced the phosphorylation of HIF-1alpha, which was inhibited by KN93. CONCLUSIONS AND IMPLICATIONS: Our results suggest that artemisinin and parthenolide may act as SERCA inhibitors and, like other SERCA inhibitors, induce resistance to doxorubicin in human colon cancer cells, via the CaMKII-dependent activation of HIF-1alpha and the induction of Pgp.

PMID: 19298255 [PubMed - indexed for MEDLINE]


...may synergize with Cyclophosphamide and others, in lung cancer:

Cancer Chemother Pharmacol. 2009 Sep 16. [Epub ahead of print]
Dihydroartemisinin improves the efficiency of chemotherapeutics in lung carcinomas in vivo and inhibits murine Lewis lung carcinoma cell line growth in vitro.

Zhou HJ, Zhang JL, Li A, Wang Z, Lou XE.
Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, 388 Yuhang'tang Road, Hangzhou, Zhejiang, 310058, People's Republic of China, zhouhj_zhouhj@yahoo.com.
PURPOSE: Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, has exhibited the strongest antimalarial activity among the derivatives of artemisinin. There is growing evidence that DHA has some impact against tumors. Our purpose was to evaluate in vitro antitumoral properties of DHA in the murine Lewis lung carcinoma (LLC) cell line. At the same time, we observed the therapeutic effect of DHA combined with cyclophosphamide (CTX) in the LLC and combined with cisplatin (CDDP) in the human non-small cell lung cancer A549 xenotransplanted carcinoma in vivo. METHODS: Cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method, apoptosis was measured by AO/EB double staining and flow cytometry. The expression of vascular endothelial growth factor (VEGF) receptor KDR/flk-1 was analyzed by western blotting and RT-PCR. In vivo activity of DHA combined with CTX or CDDP was assayed through tumor growth and metastasis. RESULTS: Dihydroartemisinin exhibited high anti-cancer activity in LLC cell line. DHA also induced apoptosis of LLC cells and influenced the expression of VEGF receptor KDR/flk-1. Furthermore, in both tumor xenografts, a greater degree of growth inhibition was achieved when DHA and chemotherapeutics were used in combination. The affection by DHA combined CTX on LLC tumor metastasis was significant. CONCLUSIONS: Dihydroartemisinin is a potent compound against LLC cell line in vitro. In vivo, the combination strategy of DHA and chemotherapeutics holds promise for the treatment of relatively large and rapidly growing lung cancers.

PMID: 19756601 [PubMed - as supplied by publisher]

Int Immunopharmacol. 2010 Sep;10(9):1055-61. Epub 2010 Jul 2.
A comparison of low-dose cyclophosphamide treatment with artemisinin treatment in reducing the number of regulatory T cells in murine breast cancer model.

Langroudi L, Hassan ZM, Ebtekar M, Mahdavi M, Pakravan N, Noori S.
Department of Immunology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran. lnlangroudi@modares.ac.ir

AbstractBACKGROUND: Artemisinin (ART) is a sesquiterpene lactone. Possessing an endoperoxide bridge is unique among antimalarial drugs, and now much attention is focused on the anti-cancer properties of ART. In this study we aimed at the immunomodulatory effects of artemisinin in the treatment of breast cancer in comparison to the conventional anti-cancer drug, cyclophosphamide (CTX).
METHODS: We examined delayed-type hypersensitivity, antibody and IL-4 and IFN gamma production, tumour volume, tumour infiltrated regulatory T cells (Treg) and spleen lymphocyte proliferation assay. Briefly three groups of five 4-6 week old female Balb/c tumour-bearing mice (mouse mammary tumour) were treated with 2.8 mg/kg ART and 20mg/kg CTX intraperitoneally for 20 consecutive days. Tumour volume was measured using a digital vernier calliper (with accuracy of 0.01). Mice were sacrificed and percentage of tumour infiltrating Tregs were obtained using flow cytometry (BD, USA). Proliferation of splenocytes was obtained using BrdU proliferation assay (Roche).
RESULTS: Our results showed that ART can reduce the number of Tregs in tumour stroma (P-value or=0.05) and control. Furthermore ART increased IFN gamma/IL-4 ratio produced in splenocyte culture (P-value or=0.05).
DISCUSSION: Cancer is a multi-factorial disease which needs a multi-approach treatment. Early accumulation of Treg cells in the tumour tissue correlates with tumour progression and is an indication of bad prognosis. According to the obtained results, ART can reduce the number of Tregs. We suggest using artemisinin, with its dual action mechanism. It can effectively kill cancer cells along with reducing the suppressive microenvironment.

PMID: 20601187 [PubMed - in process]

Site with background and various protocols/stragegies:


Biochem Pharmacol. 2010 Mar 3. [Epub ahead of print]
Dihydroartemisinin accelerates c-MYC oncoprotein degradation and induces apoptosis in c-MYC-overexpressing tumor cells.

Lu JJ, Meng LH, Shankavaram UT, Zhu CH, Tong LJ, Chen G, Lin LP, Weinstein JN, Ding J.
Division of Anti-tumor Pharmacology, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zu Chong Zhi Rd., Shanghai 201203, PR China.
Artemisinin and its derivatives (ARTs) are effective antimalarial drugs and also possess profound anticancer activity. However, the mechanism accounted for its distinctive activity in tumor cells remains unelucidated. We computed Pair-wise Pearson correlation coefficients to identify genes that show significant correlation with ARTs activity in NCI-55 cell lines using data obtained from studies with HG-U133A Affymetrix chip. We found c-myc is one of the genes that showed highest positive correlation coefficients among the probe sets analyzed (r=0.585, P<0.001). Dihydroartemisinin (DHA), the main active metabolite of ARTs, induced significant apoptosis in HL-60 and HCT116 cells that express high levels of c-MYC. Stable knockdown of c-myc abrogated DHA-induced apoptosis in HCT116 cells. Conversely, forced expression of c-myc in NIH3T3 cells sensitized these cells to DHA-induced apoptosis. Interestingly, DHA irreversibly down-regulated the protein level of c-MYC in DHA-sensitive HCT116 cells, which is consistent to persistent G1 phase arrest induced by DHA. Further studies demonstrated that DHA accelerated the degradation of c-MYC protein and this process was blocked by pretreatment with the proteasome inhibitor MG-132 or GSK 3beta inhibitor LiCl in HCT116 cells. Taken together, ARTs might be useful in the treatment of c-MYC-overexpressing tumors. We also suggest that c-MYC may potentially be a biomarker candidate for prediction of the antitumor efficacies of ARTs. Copyright © 2010. Published by Elsevier Inc.

PMID: 20206143 [PubMed - as supplied by publisher]

Extensive Discussion of human dosing, synergies, interactions etc at site about Canine cancer: LINK

Radiation releases iron stored in cancer cells into surrounding tissue. Therefore, it is recommended that it be used before radiation treatments, be discontinued during radiation treatments, and not resumed until two months after the last radiation treatment.


Artemisinin was tested in combination with 22 chemotherapy drugs and was found to enhance the drugs’ effectiveness. If used in conjunction with chemotherapy, it should be taken several hours after the chemotherapy treatment ends. (Artemisinin does not alleviate possible chemotherapy side effects.)
Zhong Xi Yi Jie He Xue Bao. 2008 Feb;6(2):134-8.
[Artesunate combined with vinorelbine plus cisplatin in treatment of advanced non-small cell lung cancer: a randomized controlled trial]

[Article in Chinese]
Zhang ZY, Yu SQ, Miao LY, Huang XY, Zhang XP, Zhu YP, Xia XH, Li DQ.
Department of Respiratory Medicine, Dongguan Kuanghua Hospital, Dongguan, Guangdong Province, China.
OBJECTIVE: To our knowledge, there has been no clinical report of artesunate in the treatment of lung cancer. This study was designed to compare the efficacy and toxicity of artesunate combined with NP (a chemotherapy regimen of vinorelbine and cisplatin) and NP alone in the treatment of advanced non-small cell lung cancer (NSCLC). METHODS: One hundred and twenty cases of advanced NSCLC were randomly divided into simple chemotherapy group (control group, n=60) and combined artesunare with chemotherapy group (trial group, n=60). Patients in the control group were treated with NP regimen, including vinorelbine (25 mg/m(2), once-a-day intravenous injection, at the 1st and 8th day) and cisplatin (25 mg/m(2), once-a day intravenous drip, at the 2nd to 4th day). Patients in the trial group were treated with the basal therapy NP (in the same method and doses as control group) and artesunate (120 mg, once-a-day intravenous injection, from the 1st day to 8th day, for 8 days). At least two 21-day-cycles of treatment were performed. The short-term survival rate, disease controlled rate (DCR), time to progression (TTP), mean survival time (MST) and 1-year survival rate were analyzed as the primary end points, and the toxicity and safety were estimated. RESULTS: There were no significant differences in the short-term survival rate, MST and 1-year survival rate between the trial group and the control group, which were 45.1% and 34.5%, 44 weeks and 45 weeks, 45.1% and 32.7%, respectively (P>0.05). The DCR of the trial group (88.2%) was significantly higher than that of the control group (72.7%) (P<0.05), and the trial group's TTP (24 weeks) was significantly longer than that of the control group (20 weeks) (P<0.05). No significant difference was found in toxicity between the two groups, such as myelosuppression and digestion reaction (P>0.05). CONCLUSION: Artesunate can be used in the treatment of NSCLC. Artesunate combined with NP can elevate the short-term survival rate and prolong the TTP of patients with advanced NSCLC without extra side effects.

PMID: 18241646 [PubMed - in process]


Extract of Chinese Herb Fights Cancer
This Malaria Drug Also Kills Cancer Cells
By Robert Jay Rowen M.D.


Remember our old friend hydrogen peroxide? All peroxides share a common feature. In the presence of free iron, they break down to form highly reactive oxygen-based free radicals. Malaria is a parasite (Plasmodium) that infects the iron-rich red blood cell and accumulates iron. While the body avidly shields iron in a bound-up state (hemoglobin, enzymes, etc.), excess iron accumulates in the parasite, and the accumulation allows some iron to spill out of the bound state and become free. When the artemisinin products contact the iron – boom! A huge burst of free radicals is unleashed, virtually blowing up the cell harboring the free iron and destroying the parasite.
Some seven years ago, Dr. Lai, aware of the high accumulation of iron in cancer cells, wondered if this same mechanism might work in cancer cells, wondered if this same mechanism might work in cancer treatment. He and his colleague, Dr. Singh, conducted experiments in laboratory cancer cells documenting a 100% kill rate of breast-cancer cells in just hours. More importantly, it left normal breast cells and white blood cells unscathed.
Then, one year ago, an article appeared in a major cancer journal demonstrating significant artemisinin anticancer activity in a wide variety of laboratory cultured cancer cells. But astonishingly, cancer's resistance to common chemotherapy drugs shows no such resistance to artemisinin. It does not have the chemical structure a cancer cell requires to develop resistance! (This was reported recently in the International Journal of Oncology 18; 767-773, 2001 by Efferth, et al.)

The anti-malarial artesunate is also active against cancer (2001)

(includes charted cell study comparisons of Artesunate to chemo in various cancers and many reference studies at that time)

HTML version



Dr. Hoang of Hanoi, whose family of physicians has used artemisinin for 10 years reported that he has had a 50-60% long term remission rate with 400 cancer patients when artemisinin is used with a comprehensive integrative cancer strategy. There are 3 common artemeia derivatives, with distinct properties.

Artesunate is water soluble and may be the most active and least toxic, but it has the shortest life within the body. Artemether is oil or lipid soluble and has the longest half-life and the highest toxicity, but that is related to the high dosages, which are not necessary. Its advantage is its ability to cross the blood brain barrier to reach cancers of the brain and nervous system. Artemisinin is the active parent compound of the plant. It has an intermediate half-life, is very safe and also crosses the blood brain barrier. The first 2 are slightly altered synthetic derivatives of artemesinin.

Dr. Narenda Singh, Professor pf Bioengineering at the University of Washington reports the best treatment may be a combination based on a lab experiment. He suggests equal parts of artemisinin and artemether to provide .5 to 2 mg/Kg of weight for each form, taken once daily before bed(away from any residual iron left in the stomach from the evening meal).

Dr. Hoang reports that he has been using 500mg of oral artemesinin taken twice a day by itself with marked success.

The product is best taken on an empty stomach with some natural fat to aid absorption. Any Iron present from other foods may neutralise the peroxides. Milk is a food with minimal iron content. Whole milk, cottage cheese or yogurt have ample fat to aid absorption. Dr. Rowen feels that cod liver oil and conjugated linoleic acid (CLA) will assist absorption and provide additional therapeutic benefit from omega-3 fats and vitamin D.

Dr. Singh has tested some artemesinin products and found only 10-20% of the anticancer activity against cultured cancer cells. Allergy Research Group (800-545-9960) has a high grade artemisinin confirmed by independent lab analysis. It should be used in conjunction with a comprehensive cancer strategy to build the immune system with the help of an integrative medicine physician or an open minded oncologist.
For more information, contact Lai at 206-543-1071 or hlai@u.washington.edu


There are three common Artemesia derivatives - Artesunate is water soluble and may be the most active and the least toxic, but it has the shortest life within the body. Artemether is oil or lipid soluble and has the longest half-life. It also has the most toxicity (but this is related to rather high dosages, which are not necessary. Its big advantage is that it can cross the blood-brain barrier to reach cancers in the nervous system. Artemisinin is the active parent compound of the plant. It has an intermediate half-life, is very safe, and also can cross the blood-brain barrier.The first two are slightly altered semi-synthetic derivatives of artemisinin, the concentrated and purified active agent. Dr. Singh reports that a combination of the forms may be the very best treatment due to these different properties (based on a lab experiment). Thus, he feels the best preparation will contain artemisinin and artemether to provide a dose of 0.5-2 mg/Kg of each form once daily before bed (away from any residual iron left in the stomach from the evening meal). Dr. Hoang used 500 mg twice daily of oral artemisinin with good success. The product is best taken on an empty stomach with some natural fat to enhance absorption. Any iron present from residual food may neutralize the peroxides. Milk is one of the few foods with minimal iron. Whole milk, cottage cheese, or yogurt have ample fat to enhance absorption.

Volume 231, Issue 1, Pages 43-48 (8 January 2006)
Oral artemisinin prevents and delays the development of 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast cancer in the rat

Henry Lai, Narendra P. Singh
Received 30 October 2004; accepted 14 January 2005.

Artemisinin, a compound isolated from the sweet wormwood Artemisia annua L., has previously been shown to have selective toxicity towards cancer cells in vitro. In the present experiment, we studied the potential of artemisinin to prevent breast cancer development in rats treated with a single oral dose (50mg/kg) of 7,12-dimethylbenz[a]anthracene (DMBA), known to induce multiple breast tumors. Starting from the day immediately after DMBA treatment, one group of rats was provided with a powdered rat-chow containing 0.02% artemisinin, whereas a control group was provided with plain powdered food. For 40 weeks, both groups of rats were monitored for breast tumors. Oral artemisinin significantly delayed (P<.002) and in some animals prevented (57% of artemisinin-fed versus 96% of the controls developed tumors, P<.01) breast cancer development in the monitoring period. In addition, breast tumors in artemisinin-fed rats were significantly fewer (P<.002) and smaller in size (P<.05) when compared with controls. Since artemisinin is a relatively safe compound that causes no known side effects even at high oral doses, the present data indicate that artemisinin may be a potent cancer-chemoprevention agent.

Expert Rev Mol Med. 2009 Oct 30;11:e32.
Anticancer activities of artemisinin and its bioactive derivatives.

Firestone GL, Sundar SN.
Department of Molecular and Cell Biology and The Cancer Research Laboratory, The University of California at Berkeley, CA 94720-3200, USA. glfire@berkeley.edu
Artemisinin, a sesquiterpene lactone derived from the sweet wormwood plant Artemisia annua, and its bioactive derivatives exhibit potent anticancer effects in a variety of human cancer cell model systems. The pleiotropic response in cancer cells includes growth inhibition by cell cycle arrest, apoptosis, inhibition of angiogenesis, disruption of cell migration, and modulation of nuclear receptor responsiveness. These effects of artemisinin and its derivatives result from perturbations of many cellular signalling pathways. This review provides a comprehensive discussion of these cellular responses, and considers the ramifications for the potential development of artemisinin-based compounds in anticancer therapeutic and preventative strategies.

PMID: 19883518 [PubMed - indexed for MEDLINE]

J Biol Chem. 2009 Jan 23;284(4):2203-13. Epub 2008 Nov 17.

Artemisinin blocks prostate cancer growth and cell cycle progression by disrupting Sp1 interactions with the cyclin-dependent kinase-4 (CDK4) promoter and inhibiting CDK4 gene expression.

Willoughby JA Sr, Sundar SN, Cheung M, Tin AS, Modiano J, Firestone GL.
Department of Molecular and Cell Biology and Cancer Research Laboratory, University of California at Berkeley, Berkeley, California 94720-3200, USA.
Artemisinin, a naturally occurring component of Artemisia annua, or sweet wormwood, is a potent anti-malaria compound that has recently been shown to have anti-proliferative effects on a number of human cancer cell types, although little is know about the molecular mechanisms of this response. We have observed that artemisinin treatment triggers a stringent G1 cell cycle arrest of LNCaP (lymph node carcinoma of the prostate) human prostate cancer cells that is accompanied by a rapid down-regulation of CDK2 and CDK4 protein and transcript levels. Transient transfection with promoter-linked luciferase reporter plasmids revealed that artemisinin strongly inhibits CDK2 and CDK4 promoter activity. Deletion analysis of the CDK4 promoter revealed a 231-bp artemisinin-responsive region between -1737 and -1506. Site-specific mutations revealed that the Sp1 site at -1531 was necessary for artemisinin responsiveness in the context of the CDK4 promoter. DNA binding assays as well as chromatin immunoprecipitation assays demonstrated that this Sp1-binding site in the CDK4 promoter forms a specific artemisinin-responsive DNA-protein complex that contains the Sp1 transcription factor. Artemisinin reduced phosphorylation of Sp1, and when dephosphorylation of Sp1 was inhibited by treatment of cells with the phosphatase inhibitor okadaic acid, the ability of artemisinin to down-regulate Sp1 interactions with the CDK4 promoter was ablated, rendering the CDK4 promoter unresponsive to artemisinin. Finally, overexpression of Sp1 mostly reversed the artemisinin down-regulation of CDK4 promoter activity and partially reversed the cell cycle arrest. Taken together, our results demonstrate that a key event in the artemisinin anti-proliferative effects in prostate cancer cells is the transcriptional down-regulation of CDK4 expression by disruption of Sp1 interactions with the CDK4 promoter.

PMID: 19017637 [PubMed - indexed for MEDLINE]

Carcinogenesis. 2008 Dec;29(12):2252-8. Epub 2008 Sep 10.
Artemisinin selectively decreases functional levels of estrogen receptor-alpha and ablates estrogen-induced proliferation in human breast cancer cells.

Sundar SN, Marconett CN, Doan VB, Willoughby JA Sr, Firestone GL.
Department of Molecular and Cell Biology and the Cancer Research Laboratory, University of California at Berkeley, Berkeley, CA 94720, USA.
MCF7 cells are an estrogen-responsive human breast cancer cell line that expresses both estrogen receptor (ER) alpha and ERbeta. Treatment of MCF7 cells with artemisinin, an antimalarial phytochemical from the sweet wormwood plant, effectively blocked estrogen-stimulated cell cycle progression induced by either 17beta-estradiol (E(2)), an agonist for both ERs, or by propyl pyrazole triol (PPT), a selective ERalpha agonist. Artemisinin strongly downregulated ERalpha protein and transcripts without altering expression or activity of ERbeta. Transfection of MCF7 cells with ERalpha promoter-linked luciferase reporter plasmids revealed that the artemisinin downregulation of ERalpha promoter activity accounted for the loss of ERalpha expression. Artemisinin treatment ablated the estrogenic induction of endogenous progesterone receptor (PR) transcripts by either E(2) or PPT and inhibited the estrogenic stimulation of a luciferase reporter plasmid driven by consensus estrogen response elements (EREs). Chromatin immunoprecipitation assays revealed that artemisinin significantly downregulated the level of endogeneous ERalpha bound to the PR promoter, whereas the level of bound endogeneous ERbeta was not altered. Treatment of MCF7 cells with artemisinin and the pure antiestrogen fulvestrant resulted in a cooperative reduction of ERalpha protein levels and enhanced G(1) cell cycle arrest compared with the effects of either compound alone. Our results show that artemisinin switches proliferative human breast cancer cells from expressing a high ERalpha:ERbeta ratio to a condition in which ERbeta predominates, which parallels the physiological state linked to antiproliferative events in normal mammary epithelium.

PMID: 18784357 [PubMed - indexed for MEDLINE]


Ann Neurol. 2006 Apr;59(4):725-6.
Toxic brainstem encephalopathy after artemisinin treatment for breast cancer.

White NJ, Ashley EA, Nosten F.
Comment on:
PMID: 16566014 [PubMed - indexed for MEDLINE]

Crit Rev Toxicol. 2010 Feb 16. [Epub ahead of print]
Toxicity of the antimalarial artemisinin and its dervatives.

Efferth T, Kaina B.
Department of Pharmaceutical Biology, Institute of Pharmacy and Biochemistry, University of Mainz, Mainz, Germany.
As long as no effective malaria vaccine is available, chemotherapy belongs to the most important weapons fighting malaria. One of the most promising new drug developments is the sesquiterpene artemisinin (ARS) and its derivatives, e.g., artemether, arteether, and sodium artesunate. Large clinical studies and meta-analyses did not show serious side effects, although proper monitoring of adverse effects in developing countries might not be a trivial task. There is a paucity of large-scale clinical trials suitable to detect rare but significant toxicity. Therefore, a final and definitive statement on the safety of artemisinins still cannot be made. In contrast, animal experiments show considerable toxicity upon application of artemisinins. In the present review, the authors give a comprehensive overview on toxicity studies in cell culture and in animals (mice, rats, rabbits, dogs, monkeys) as well as on toxicity reported in human clinical trials. The authors emphasize the current knowledge on neurotoxicity, embryotoxicity, genotoxicity, hemato- and immunotoxicity, cardiotoxicity, nephrotoxicity, and allergic reactions. The lesson learned from animal and human studies is that long-term availability rather than short-term peak concentrations of artemisinins cause toxicity. Rapid elimination of artemisinins after oral intake represents a relatively safe route of administration compared to delayed drug release after intramuscular (i.m.) injection. This explains why considerable toxicities were found in the majority of animal experiments, but not in human studies. In addition, there are drug-related differences, i.e., intramuscular application of artemether or arteether, but not to artesunate, which is safe and gives good profiles after i.m. administration in severe malaria. Although there is no need to increase doses of artemisinins for uncomplicated malaria, this has to be taken into account for cerebellar involvement in severe malaria. It might also be important in determining dose limitations for treatment of other diseases such as cancer.

PMID: 20158370 [PubMed - as supplied by publisher]

Toxicol Lett. 2004 Mar 1;147(2):99-107.
Artemisinin derivatives: toxic for laboratory animals, safe for humans?

Gordi T, Lepist EI.
Department of Pharmaceutics, School of Pharmacy, State University of New York at Buffalo, Buffalo, NY 14260, USA. tgordi@buffalo.edu
Comment in:
A discrepancy seems to prevail with regard to the toxicity and safety of the artemisinin family of antimalarials. While these compounds have been found to be virtually void of any serious side effects in humans, their neurotoxicity in animal models has raised concerns about their use. In this paper, we present selected examples of both pre-clinical and clinical studies dealing with adverse effects of artemisinin drugs. We suggest that the prolonged presence of artemisinins upon slow release from oil-based intramuscular formulations is the main cause of the observed toxicity in laboratory animals. In contrast, oral intake of these compounds, which is by far the most common formulation used for treatment of malaria patients, results in rapid clearance of these drugs and is thus unlikely to cause any toxicity in human subjects. Another plausible factor may be the relatively high doses of artemisinin compounds used in animal studies. In conclusion, the observation of the toxicity of artemisinin compounds in animals, but not in humans, is most likely due to different pharmacokinetic profiles after different routes of administrations.

PMID: 14757313 [PubMed - indexed for MEDLINE]

J Cancer Res Clin Oncol. 2009 Nov 26. [Epub ahead of print]
Growth inhibitory effects of dihydroartemisinin on pancreatic cancer cells: involvement of cell cycle arrest and inactivation of nuclear factor-kappaB.

Chen H, Sun B, Wang S, Pan S, Gao Y, Bai X, Xue D.
Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, 150001, Harbin, China, chenhuahyd@yahoo.com.cn.
PURPOSE: In a recent publication, we have shown that dihydroartemisinin (DHA), a derivative of antimalaria drug artemisinin, inhibits growth of pancreatic cancer cells in vitro and in vivo mediated by its anti-proliferative and pro-apoptotic effects. As it has been shown that the apoptosis might be induced due to cell cycle arrest, and that transcriptional factor nuclear factor-kappa B (NF-kappaB) plays vital roles in the apoptosis of pancreatic cancer cells, we extend our study to investigate the effects of DHA on cell cycle progression and NF-kappaB activity in pancreatic cancer cells to further reveal the anticancer effects of DHA on pancreatic cancer. METHODS: Cell cycle progression was determined by propidium iodide staining and flow cytometry. Changes in the expression of cell cycle-associated proteins were detected using Western blot analysis. Measurement of NF-kappaB activity was performed with immunoblot analyzing the nuclear protein expression of NF-kappaB/p65 and ELISA detecting the NF-kappaB DNA-binding activity. RESULTS: The treatment with DHA resulted in a dose-dependent G(0)/G(1) cell cycle arrest and regulated the expression of some cyclins, cdks and cdk inhibitors that involved in the G(0)/G(1) cell cycle progression such as cyclin E, cdk2, cdk4 and p27(Kip1) in pancreatic cancer BxPC-3 and AsPC-1 cells. The translocation and DNA-binding activity of NF-kappaB were inhibited in DHA-treated cells in a dose-dependent manner, indicated the inactivation effects of DHA in pancreatic cancer cells. CONCLUSIONS: Together with our previous observations, our data show that DHA induces cell cycle arrest and apoptosis in pancreatic cancer cells, and this effect might be due to inhibition of NF-kappaB signaling. We suggest that DHA could be developed as a novel agent against pancreatic cancer.

PMID: 19941148 [PubMed - as supplied by publisher]

Cancer Chemother Pharmacol. 2010 Apr;65(5):895-902. Epub 2009 Aug 19.
Artesunate induces oncosis-like cell death in vitro and has antitumor activity against pancreatic cancer xenografts in vivo.

Du JH, Zhang HD, Ma ZJ, Ji KM.
Central Laboratory, Nanshan Hospital, Guangdong Medical College, 518052, Shenzhen, Guangdong Province, People's Republic of China.
Pancreatic cancer is highly resistant to the currently available chemotherapeutic agents. Less than 5% of patients diagnosed with this disease could survive beyond 5 years. Thus, there is an urgent need for the development of novel, efficacious drugs that can treat pancreatic cancer. Herein we report the identification of artesunate (ART), a derivative of artemisinin, as a potent and selective antitumor agent against human pancreatic cancer cells in vitro and in vivo. ART exhibits selective cytotoxic activity against Panc-1, BxPC-3 and CFPAC-1 pancreatic cancer cells with IC(50) values that are 2.3- to 24-fold less than that of the normal human hepatic cells (HL-7702). The pan caspase inhibitor zVAD-fmk did not inhibit the cytotoxic activity of ART. Electron microscopy of ART-treated cells revealed severe cytoplasmic swelling and vacuolization, swollen and internally disorganized mitochondria, dilation (but not fragmentation) of the nuclei without chromatin condensation, and cell lysis, yielding a morphotype that is typical of oncosis. The ART-treated cells exhibited a loss of mitochondrial membrane potential (DeltaPsim) and ART-induced cell death was inhibited in the presence of the reactive oxygen species (ROS) scavenger N-acetyl-cysteine (NAC). Importantly, ART produced a dose-dependent tumor regression in an in vivo pancreatic cancer xenografts model. The in vivo antitumor activity of ART was similar to that of gemcitabine. Taken together, our study suggests that ART exhibits antitumor activity against human pancreatic cancer via a novel form of oncosis-like cell death, and that ART should be considered a potential therapeutic candidate for treating pancreatic cancer.

PMID: 19690861 [PubMed - in process]

Cancer Biol Ther. 2010 May 18;9(10). [Epub ahead of print]
Dihydroartemisinin upregulates death receptor 5 expression and cooperates with TRAIL to induce apoptosis in human prostate cancer cells.

He Q, Shi J, Shen XL, An J, Sun H, Wang L, Hu YJ, Sun Q, Fu LC, Sheikh MS, Huang Y.
Department of Pharmacology, State University of New York, Upstate Medical University, Syracuse, NY, USA.
Dihydroartemisinin (DHA) is a derivative of artemisinin and is an effective anti-malaria therapeutic used worldwide. In this paper, we report that DHA is as a potential anti-cancer drug for prostate cancer. Our data indicate that DHA suppresses the PI3-K/Akt and ERK cell survival pathways and triggers the induction of death receptor DR5 and activation of extrinsic and intrinsic cell death signaling. DHA-mediated DR5 induction appears to occur via increased transcriptional activity of DR5 promoter. Our data also show that, while DHA has strong cytotocixity in tumor cells, it exhibits minimal cytotoxic effects on normal prostate epithelial cells. Our studies also demonstrate that DHA worked cooperatively with death ligand TRAIL. Combination of DHA and TRAIL significantly enhanced cell killing above that noted with a single agent alone. Based on these results, we propose a novel idea of developing DHA alone and/or in combination with TRAIL for the treatment of prostate cancer.

PMID: 20224297 [PubMed - as supplied by publisher]

Int J Cancer. 2010 Mar 15. [Epub ahead of print]
First evidence that the anti-malarial drug Artesunate inhibits invasion and in vivo metastasis in lung cancer by targeting essential extracellular proteases.

Rasheed SA, Efferth T, Asangani IA, Allgayer H.
Department of Experimental Surgery and Molecular Oncology of Solid Tumors, Medical Faculty Mannheim, University of Heidelberg, and German Cancer Research Center (DKFZ)- Heidelberg, Mannheim, Germany.
Despite progress in treatment, progressive non-small cell lung cancer (NSCLC) still limits survival dramatically, and novel therapeutic compounds are needed. Initial investigations suggest that Artesunate (ART), an anti-malarial drug, has anti-proliferative capacities. However, anti-invasive and anti-metastatic properties of ART in cancer have never been explored. Therefore, this first study was performed to (1) investigate if ART is able to inhibit invasion and metastasis in NSCLC, and (2) to identify first molecular targets and mechanisms mediating this ability. ART significantly impaired matrigel invasion of 6 NSCLC cell lines, and inhibited urokinase-type plasminogen activator (u-PA) activity, -protein and -mRNA-expression. Furthermore, in a PCR-metastasis array, ART inhibited the expression of several matrix metallo-proteinases (MMPs), especially MMP-2 and MMP-7 mRNA/-protein. In luciferase reporter assays, ART downregulated MMP-2-, MMP-7-, and u-PA-promoter/-enhancer activity, in parallel to AP-1- and NF-kB-transactivation. Si-RNA knockdown of u-PA, MMP-2 and MMP-7 abolished ART's ability to inhibit invasion, confirming their role as essential mediators. In vivo, ART significantly impaired primary tumor growth and metastasis in the chicken embryo metastasis (CAM) model. In conclusion, this is the first study to show that ART considerably suppresses invasion and metastasis in NSCLC, specifically targeting transcription of u-PA, MMP-2 and MMP-7, prompting immediate studies on Artesunate as a novel therapeutic in NSCLC. (c) 2010 UICC.

PMID: 20232396 [PubMed - as supplied by publisher]

ARCO Artemisinin/Napthoquinone tablets: http://www.ngcplc.com/arco/index.html
ARCO® Tablet is the newest generation of high efficacy oral fixed-dose Artemisinin-based Combination Therapy (ACT) antimalarials available in the world. Arco® tablet is light-yellow coloured combination tablet of 78.3 mg of Naphthoquine phosphate (equivalent to 50 mg of Naphthoquine) and 125 mg of Artemisinin in each tablet.
Teen researches Artemesinin for cancer:

Mom's treatment history (link)
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Old 01-02-2010, 10:33 AM   #2
Ellie F
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Re: Artemisinin (anti-malarial, anti-cancer)

Thanks Rich for posting this comprehensive review. Karen T has used this with success (first time she has had stable disease and it has lasted 9 months). The low toxicity is encouraging and I wonder if with low volume disease the efficacy may be even better.
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Old 01-02-2010, 11:39 AM   #3
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Re: Artemisinin (anti-malarial, anti-cancer)

That's great! I couldn't find Karen T. Please have her comment with details if you can reach her.
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Old 04-30-2010, 06:33 AM   #4
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Re: Artemisinin (anti-malarial, anti-cancer)

Thank you, Rich, for pointing this thread to me. Do you know of anyone here taking Wormwood supplements? What is the recommended dosage? My hear of Herceptin is coming up, and I'd love to be on as many security blankets as possible.
ER+ (30%)/PR-/HER-2+, stage 3

Diagnosed on 02/18/09 at 38 with a huge 12x10 cm tumor, after a 6 month delay. Told I was too young and had no risk factors. Found swollen node during breastfeeding.
March-August 09: neo-adjuvant chemo, part of a trial at Stanford (4 DD A/C, 4 Taxotere with daily Tykerb), loading dose of Herceptin
08/12/09 - bye bye boobies (bilateral mastectomy)
08/24/09 - path report shows 100 % success in breast tissue (no cancer there, yay!), 98 % success in lymphatic invasion, and even though 11/13 nodes were still positive, > 95 % of the tumor in them was killed. Hoping for the best!
September-October 09: rads with daily Xeloda
02/25/10 - Cholecystectomy
05/27/10 - Bone scan clear
06/14/10 - CT scan clear, ovarian cyst found
07/27/10 - Done with Herceptin!
02/15/11 - MVA-BN HER-2 vaccine trial
03/15/11 - First CA 15-3: 12.7 and normal, yay!
10/01/11 - Bone scan and CT scan clear, fatty liver found
now on Tamoxifen and Aspirin

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Old 09-18-2010, 03:24 PM   #5
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Re: Artemisinin (anti-malarial, anti-cancer)

Mol Immunol. 2010 Apr;47(7-8):1579-84. Epub 2010 Feb 9.
Tehranolide molecule modulates the immune response, reduce regulatory T cell and inhibits tumor growth in vivo.

Noori S, Taghikhani M, Hassan ZM, Allameha A, Mostafaei A.
Department of Biochemistry, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.



Tehranolide named as new type of a sesquiterpene lactone with an endoperoxide group which purified from Artemisia diffusa and having similar structure to Artemisinin. Tehranolide is hypothesized to possess effects akin to Artemisinin, which is active against cancer cells. In the present research we emphasized on the direct correlation between the tumor sizes, immune response; including cytokin network, T regulatory cells and Tehranolide intraperitoneally injected Tehranolide. In this study, Tehranolide was purified from Artemisia difussa. First we evaluated the effects of Tehranolide on cell growth inhibition (in vitro) by MTT assay and second investigated the immune responses, these include measuring tumor growth in the female Balb/c mice transplanted with spontaneous mouse mammary tumor and treated with Tehranolide, splenocyte proliferation detected by using the BrdU kit, measurement of cytokine profile by ELISA and analysis of T-lymphocytes subpopulation in spleen by Flow cytometry. Our results showed a significant (p<0.05) decrease in the tumor volume and the level of IL-4 in the animals treated with Tehranolide, compared to untreated group. In addition, a significant (p<0.05) increase in the lymphocytes proliferation and the level of IFN-gamma in the animals treated with Tehranolide in comparison with control group. Furthermore, we regulate the regulatory T cells in order to improve the outcome of cancer immunotherapy. The measurement of splenic CD4(+)CD25(+)Foxp3(+) T lymphocytes indicated that Tehranolide significantly (p<0.05) decreased the number of these lymphocytes. These findings show that the use of Tehranolide molecule represents a novel strategy with major suggestions for cancer therapy approaches.

PMID: 20138670 [PubMed - indexed for MEDLINE]
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Old 09-18-2010, 03:24 PM   #6
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Re: Artemisinin (anti-malarial, anti-cancer)

.................................................. ........
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Old 11-01-2011, 03:35 AM   #7
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Re: Artemisinin (anti-malarial, anti-cancer)

bumping this up

35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies

Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..

superior vena cava blocked: stent but face remains puffy

April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.

Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.

'Under no circumstances should you lose hope..' Dalai Lama
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Old 11-01-2011, 11:23 AM   #8
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Re: Artemisinin (anti-malarial, anti-cancer)

In March i made up my own tinicture green walnuts soaked in vodka and wormwood plant. Which i now growen in the garden. I was not on any systemic treatment and had bone mets my last scan showed the bone mets had dyed and my bones were healling much to my Onc suprise he was not sure why and could only put it down to a heral brew. As i have brain mets i'm going to get back on my brew. This is a really intersting article thanks. Jacqui
Oct 2009 Masectomy 6 cm Tumor . Sentinal node biopsy , Node Positive . Her2 + er/pr -.
Nov 2009 X3 Taxane and Herceptin, X3 FEC
March 2010 25 Rads
March 2010 continued on Herception untill 16 Dec 2010
May 2010 Ultra Sound .... ALL CLEAR... NED
August 2010 started vaccine trial University of Washington
7th Dec 2010 finished vaccine trial
20th Dec 2010 Port removed
3rd Feb no longer ned brain mets
23r Feb start VMAT radiation
August 2011 two new mets to brain and others starting to grow again !!!!
August start tykerb and xeloda
Dec 1 MRI all small brain mets gone. Largest shrunk by 50% only three small ones to go 17mm,8mm,6mm. Mets on there way out. Yeah
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Old 06-13-2017, 11:16 PM   #9
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Re: Artemisinin (anti-malarial, anti-cancer)

Has anyone had success using Artemisinin? Or used it and it didn't work for them? What dosage did you take? I've been using it since my recurrence, 500mg in morning and 500mg in evening on an empty stomach. Wondering if higher dose might work better.
Sept 2015: diagnosed with stage 2b breast cancer. 5.5cm tumor in left breast.
Oct 2015: began neoadjuvant infusions of herceptin and perjeta. Reduced tumor.
May 2016: lumpectomy. Didn't get clear margins.
June 2016: began Kadcyla TDM-1.
October 2016: clear PET scan. No evidence of malignancy
Oct 2016-Feb 2017: continued on Kadcyla.
Feb 2017: began Herceptin only.
May 2017: found new lump. MRI shows multi-focal 5+cm.
May 2017: began taking Artemisinin (500mg 2x/day), graviola (1300mg 2x/day, plus evening tea), CBD oil (80mg in evening), Pau D'Arco.
June 2017: in addition to above herbal medicines, added Mistletoe (orally with tincture), Turmeric, Tibetan herbs.
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