Бях помолен от англоезичен познат да подготвя списък на най-обещаващите в онко-терапията нискотоксични и нетоксични вещества, като акцентирам само върху най-важните статии, които лабораторно или клинично демонстрират тяхната антиракова активност. Намирам, че ще бъде полезно да публикувам писмото, тъй като темата е пряко свързана и с веществата, за които в новата микробиологична литература се открива, че имат и най-силната антиборелийна функция и са обещаващи в лечението на хроничната борелиоза. Връзките между раковите заболявания и хроничните инфекции (бактерии - особено борелиа и нейните биофилми, някои патогенни гъби, както и онковирусите) са добре установени. Ето едно добро обобщение: "Вярваме, че този биофилмен/перзистерен "посяващ (разсаждащ)" модел е валиден за различни микробни инфекции и ще има значително приложение за разработване на по-ефективни лечения на хронични (перзистиращи) инфекции и дори при РАК(!) като цяло. We believe this biofilm/persister seeding model to be valid for different microbial infections and will have broad implications for developing more effective treatments of persistent infections and even cancer in general.
Biofilm Structures of Borrelia burgdorferi Not Only Display More Tolerance to Lyme Antibiotics But Also Cause More Severe Pathology In a Mouse Arthritis Model: Implications for Understanding Persistence, PTLDS, and Treatment Failure
Jie Feng, Tingting Li, Ying Zhang
doi: https://doi.org/10.1101/440461
https://www.biorxiv.org/content/early/2018/10/13/440461
В линк ще приложа и pdf форма на писмото.
При интерес ще се погрижа и за пълен превод на български.
Biofilm Structures of Borrelia burgdorferi Not Only Display More Tolerance to Lyme Antibiotics But Also Cause More Severe Pathology In a Mouse Arthritis Model: Implications for Understanding Persistence, PTLDS, and Treatment Failure
Jie Feng, Tingting Li, Ying Zhang
doi: https://doi.org/10.1101/440461
https://www.biorxiv.org/content/early/2018/10/13/440461
В линк ще приложа и pdf форма на писмото.
При интерес ще се погрижа и за пълен превод на български.
Dear ...,
I have summarized here only three of the оpportunities for low-toxic/non-toxic treatment of certain oncological diseases: Tigecycline, Gemifloxacin, and Artemisinin and its derivatives.
In recent years, the oncological capabilities of fluoroquinolones have been studied carefully. In this context the quinolones' family of drugs seems to link three different biological activities - antibacterial, anticancer and antiviral profiles, and a review can also provide an insight into the different mechanisms responsible for these activities among different species. Being a fourth generation fluoroquinolone, gemifloxacin differs from others not only in its low toxicity but also in the relatively rare occurrences (if any) of side effects. The application of artemisinin is very practical, as it is now available as a dietary supplement. Over the last 30 years its anticancer, antiviral, antifungal, antiparasitic and antimalarial function has been well proven. In particular, in oncological manifestations and tumors caused by oncoviruses its selective apoptotic function against cancer cells increases considerably with a split intake of trivalent iron (a minimum of 4 hours interval in the split intake of artemisinin and iron).
In a second letter I will provide you with information about the anticancer function and application of other non-toxic substances like the powerful ATF inhibitors – disulphiram and gambogic acid. As far as they are concerned, there are already some successful clinical results, and both are included in the recommended protocol for the treatment of the most aggressive form of brain tumor – glioblastoma. Other possibilities for nontoxic cancer treatment are also some compounds with selective cytotoxicity like frankincense and myrrh essential oils (and their synergistic combination), carvacrol (from oregano essential oil), cinnamaldehyde (from cinnamon essential oil), garlic essential oil, which can be prepared in a nanoencapsulated formulation for a better delivery. (Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition. 2011. Chapter 17. Herbs and Spices in Cancer Prevention and Treatment.https://www.ncbi.nlm.nih.gov/books/NBK92774/).
Particularly important in this field are some of the penicillins and cephalosporins group antibiotics – cefoperazone + sulbactam, azlocillin, ceftriaxone, piperacillin-tazobactam etc. Not surprisingly all of these compounds (including essential oils but with improved delivery for in vivo application, because they have very low bioavailability in humans!) have the strongest antiborrelial activity and are very promising in the treatment of persistent forms of borreliosis – chronic Lyme disease. The connection between cancers and bacteria (especially borrelia and their biofilms), some pathogenic fungi (oncogenic fungi) and oncoviruses is well established.
It is well summarized and apodictically proven in a recent study (https://www.biorxiv.org/content/early/2018/10/13/440461): “We believe this biofilm/persister seeding model to be valid for different microbial infections and will have broad implications for developing more effective treatments of persistent infections and even cancer in general.”
Sincerely yours,
Yanko Marinov (23. 02. 2019)
I have summarized here only three of the оpportunities for low-toxic/non-toxic treatment of certain oncological diseases: Tigecycline, Gemifloxacin, and Artemisinin and its derivatives.
In recent years, the oncological capabilities of fluoroquinolones have been studied carefully. In this context the quinolones' family of drugs seems to link three different biological activities - antibacterial, anticancer and antiviral profiles, and a review can also provide an insight into the different mechanisms responsible for these activities among different species. Being a fourth generation fluoroquinolone, gemifloxacin differs from others not only in its low toxicity but also in the relatively rare occurrences (if any) of side effects. The application of artemisinin is very practical, as it is now available as a dietary supplement. Over the last 30 years its anticancer, antiviral, antifungal, antiparasitic and antimalarial function has been well proven. In particular, in oncological manifestations and tumors caused by oncoviruses its selective apoptotic function against cancer cells increases considerably with a split intake of trivalent iron (a minimum of 4 hours interval in the split intake of artemisinin and iron).
In a second letter I will provide you with information about the anticancer function and application of other non-toxic substances like the powerful ATF inhibitors – disulphiram and gambogic acid. As far as they are concerned, there are already some successful clinical results, and both are included in the recommended protocol for the treatment of the most aggressive form of brain tumor – glioblastoma. Other possibilities for nontoxic cancer treatment are also some compounds with selective cytotoxicity like frankincense and myrrh essential oils (and their synergistic combination), carvacrol (from oregano essential oil), cinnamaldehyde (from cinnamon essential oil), garlic essential oil, which can be prepared in a nanoencapsulated formulation for a better delivery. (Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition. 2011. Chapter 17. Herbs and Spices in Cancer Prevention and Treatment.https://www.ncbi.nlm.nih.gov/books/NBK92774/).
Particularly important in this field are some of the penicillins and cephalosporins group antibiotics – cefoperazone + sulbactam, azlocillin, ceftriaxone, piperacillin-tazobactam etc. Not surprisingly all of these compounds (including essential oils but with improved delivery for in vivo application, because they have very low bioavailability in humans!) have the strongest antiborrelial activity and are very promising in the treatment of persistent forms of borreliosis – chronic Lyme disease. The connection between cancers and bacteria (especially borrelia and their biofilms), some pathogenic fungi (oncogenic fungi) and oncoviruses is well established.
It is well summarized and apodictically proven in a recent study (https://www.biorxiv.org/content/early/2018/10/13/440461): “We believe this biofilm/persister seeding model to be valid for different microbial infections and will have broad implications for developing more effective treatments of persistent infections and even cancer in general.”
Sincerely yours,
Yanko Marinov (23. 02. 2019)
Low-toxic / non-toxic anticancer compounds.
First part: I. Tigecycline. II. Gemifloxacin. III. Artemisinin and derivatives
First part: I. Tigecycline. II. Gemifloxacin. III. Artemisinin and derivatives
I. Tigecycline
1. The Antibiotic Drug Tigecycline: A Focus on its Promising Anticancer Properties (2016)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133451/
The aim of this review is to summarize the cumulative anti-tumor evidence supporting TIG activity against different cancer types, including acute myeloid leukemia (AML), glioma, non-small cell lung cancer (NSCLC), among others. In addition, the efficacy and side effects of TIG in cancer patients are summarized in detail. Future clinical trials are also to be discussed that will evaluate the security and validate the underlying the tumor-killing properties of TIG.
2. Tigecycline Inhibits Glioma Growth by Regulating miRNA-199b-5p-HES1-AKT Pathway. (2016)
https://www.ncbi.nlm.nih.gov/pubmed/26823491
1. The Antibiotic Drug Tigecycline: A Focus on its Promising Anticancer Properties (2016)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133451/
The aim of this review is to summarize the cumulative anti-tumor evidence supporting TIG activity against different cancer types, including acute myeloid leukemia (AML), glioma, non-small cell lung cancer (NSCLC), among others. In addition, the efficacy and side effects of TIG in cancer patients are summarized in detail. Future clinical trials are also to be discussed that will evaluate the security and validate the underlying the tumor-killing properties of TIG.
2. Tigecycline Inhibits Glioma Growth by Regulating miRNA-199b-5p-HES1-AKT Pathway. (2016)
https://www.ncbi.nlm.nih.gov/pubmed/26823491
3. Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells (2017)https://www.nature.com/articles/nm.4399
Tigecycline May Selectively Target Leukemic Stem Cells in CML (2017)
Major finding: Tigecycline inhibits mitochondrial oxidative phosphorylation to target leukemic stem cells (LSC).
Concept: Tigecycline targets CD34+CD38− CML cells with little effect on nonleukemic CD34+CD38− cells.
Impact: Imatinib plus tigecycline may target LSCs and differentiated CML cells to suppress CML relapse.
http://cancerdiscovery.aacrjournals.org/content/7/11/1212.2
4. Therapeutic synergy between tigecycline and venetoclax in a preclinical model of MYC/BCL2 double-hit B cell lymphoma. (2018)
The authors found that the pair of clinically approved drugs showed synergy against the cancer and was also effective in combination with rituximab, a mainstay of current treatment for lymphoma.
http://stm.sciencemag.org/content/10/426/eaan8723?rss=1
5. Results of a Multicenter, Controlled, Randomized Clinical Trial Evaluating the Combination of Piperacillin/Tazobactam and Tigecycline in High-Risk Hematologic Patients With Cancer With Febrile Neutropenia.
Conclusion: The combination of piperacillin/tazobactam and tigecycline is safe, well tolerated, and more effective than piperacillin/tazobactam alone in febrile, high-risk, neutropenic hematologic patients with cancer. In epidemiologic settings characterized by a high prevalence of infections because of MDR microorganisms, this combination could be considered as one of the first-line empiric antibiotic therapies.http://ascopubs.org/doi/full/10.1200/JCO.2013.51.6963
6. Addition of Tigecycline to Empiric Therapy Improves Success Rate in Febrile Neutropenic Patients With Hematologic Malignancy (2014)http://www.ascopost.com/News/16145
7. Inhibition of Mitochondrial Translation as a Therapeutic Strategy for Human Acute Myeloid Leukemia. (2011) Tigecycline selectively killed leukemia stem and progenitor cells compared to their normal counterparts and also showed antileukemic activity in mouse models of human leukemia. ShRNA-mediated knockdown of EF-Tu mitochondrial translation factor in leukemic cells reproduced the antileukemia activity of tigecycline. These effects were derivative of mitochondrial biogenesis that, together with an increased basal oxygen consumption, proved to be enhanced in AML versus normal hematopoietic cells and were also important for their difference in tigecycline sensitivity.
https://www.cell.com/cancer-…/fulltext/S1535-6108(11)00398-9
8. Tigecycline use in cancer patients with serious infections: a report on 110 cases from a single institution. (2009)
https://www.ncbi.nlm.nih.gov/pubmed/19593226
9. A Phase 1 study of intravenous infusions of tigecycline in patients with acute myeloid leukemia (2016).
TG being administered over seven dose levels (50–350 mg/day). Two patients experienced DLTs related to tigecycline at the 350 mg/day level resulting in a maximal tolerated dose of tigecycline of 300 mg as a once daily infusion. Pharmacokinetic experiments showed that tigecycline had a markedly shorter half‐life in these patients than reported for noncancer patients. No significant pharmacodynamic changes or clinical responses were observed. Thus, we have defined the safety of once daily tigecycline in patients with refractory AML. Future studies should focus on schedules of the drug that permit more sustained target inhibition.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5119957/
Tigecycline May Selectively Target Leukemic Stem Cells in CML (2017)
Major finding: Tigecycline inhibits mitochondrial oxidative phosphorylation to target leukemic stem cells (LSC).
Concept: Tigecycline targets CD34+CD38− CML cells with little effect on nonleukemic CD34+CD38− cells.
Impact: Imatinib plus tigecycline may target LSCs and differentiated CML cells to suppress CML relapse.
http://cancerdiscovery.aacrjournals.org/content/7/11/1212.2
4. Therapeutic synergy between tigecycline and venetoclax in a preclinical model of MYC/BCL2 double-hit B cell lymphoma. (2018)
The authors found that the pair of clinically approved drugs showed synergy against the cancer and was also effective in combination with rituximab, a mainstay of current treatment for lymphoma.
http://stm.sciencemag.org/content/10/426/eaan8723?rss=1
5. Results of a Multicenter, Controlled, Randomized Clinical Trial Evaluating the Combination of Piperacillin/Tazobactam and Tigecycline in High-Risk Hematologic Patients With Cancer With Febrile Neutropenia.
Conclusion: The combination of piperacillin/tazobactam and tigecycline is safe, well tolerated, and more effective than piperacillin/tazobactam alone in febrile, high-risk, neutropenic hematologic patients with cancer. In epidemiologic settings characterized by a high prevalence of infections because of MDR microorganisms, this combination could be considered as one of the first-line empiric antibiotic therapies.http://ascopubs.org/doi/full/10.1200/JCO.2013.51.6963
6. Addition of Tigecycline to Empiric Therapy Improves Success Rate in Febrile Neutropenic Patients With Hematologic Malignancy (2014)http://www.ascopost.com/News/16145
7. Inhibition of Mitochondrial Translation as a Therapeutic Strategy for Human Acute Myeloid Leukemia. (2011) Tigecycline selectively killed leukemia stem and progenitor cells compared to their normal counterparts and also showed antileukemic activity in mouse models of human leukemia. ShRNA-mediated knockdown of EF-Tu mitochondrial translation factor in leukemic cells reproduced the antileukemia activity of tigecycline. These effects were derivative of mitochondrial biogenesis that, together with an increased basal oxygen consumption, proved to be enhanced in AML versus normal hematopoietic cells and were also important for their difference in tigecycline sensitivity.
https://www.cell.com/cancer-…/fulltext/S1535-6108(11)00398-9
8. Tigecycline use in cancer patients with serious infections: a report on 110 cases from a single institution. (2009)
https://www.ncbi.nlm.nih.gov/pubmed/19593226
9. A Phase 1 study of intravenous infusions of tigecycline in patients with acute myeloid leukemia (2016).
TG being administered over seven dose levels (50–350 mg/day). Two patients experienced DLTs related to tigecycline at the 350 mg/day level resulting in a maximal tolerated dose of tigecycline of 300 mg as a once daily infusion. Pharmacokinetic experiments showed that tigecycline had a markedly shorter half‐life in these patients than reported for noncancer patients. No significant pharmacodynamic changes or clinical responses were observed. Thus, we have defined the safety of once daily tigecycline in patients with refractory AML. Future studies should focus on schedules of the drug that permit more sustained target inhibition.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5119957/
II. Gemifloxacin
Several articles on the function of inhibiting the growth of cancer cells and metastases. Gemifloxacin (Factive) have good bioavailability, intracellular and CNS penetration.
1. Gemifloxacin, a Fluoroquinolone Antimicrobial Drug, Inhibits Migration and Invasion of Human Colon Cancer Cells (2013)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872387/
Full text: https://www.hindawi.com/journals/bmri/2013/159786/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872387/
„In conclusion, GMF may be a novel anticancer agent for the treatment of metastasis in colon cancer.“!!!
Several articles on the function of inhibiting the growth of cancer cells and metastases. Gemifloxacin (Factive) have good bioavailability, intracellular and CNS penetration.
1. Gemifloxacin, a Fluoroquinolone Antimicrobial Drug, Inhibits Migration and Invasion of Human Colon Cancer Cells (2013)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872387/
Full text: https://www.hindawi.com/journals/bmri/2013/159786/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872387/
„In conclusion, GMF may be a novel anticancer agent for the treatment of metastasis in colon cancer.“!!!
2. Gemifloxacin inhibits migration and invasion and induces mesenchymal–epithelial transition in human breast adenocarcinoma cells (2013)
https://www.ncbi.nlm.nih.gov/pubmed/24005829
full text:
https://www.researchgate.net/…/256448510_Gemifloxacin_inhib…
“ This study has demonstrated that GMF might be a novel anticancer agent for the prevention and treatment of metastasis in breast cancer. GMF inhibits the migration and invasion of human breast adenocarcinoma cells. GMF induces MET by reducing NF-κB and Snail activation and by increasing RKIP levels. GMF has potential clinical implication as an anti-metastatic agent for breast cancer. “
3. An study (in vitro) about gemifloxacin function in Borrelia (which is often the cause of oncological formations). Amongst the all fluoroquinolones gemifloxacine has the best function against Borrelia with the lowest MIC and MBC.
In Vitro Activities of Fluoroquinolones against the Spirochete Borrelia burgdorferi (2001)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90682/
https://www.ncbi.nlm.nih.gov/pubmed/24005829
full text:
https://www.researchgate.net/…/256448510_Gemifloxacin_inhib…
“ This study has demonstrated that GMF might be a novel anticancer agent for the prevention and treatment of metastasis in breast cancer. GMF inhibits the migration and invasion of human breast adenocarcinoma cells. GMF induces MET by reducing NF-κB and Snail activation and by increasing RKIP levels. GMF has potential clinical implication as an anti-metastatic agent for breast cancer. “
3. An study (in vitro) about gemifloxacin function in Borrelia (which is often the cause of oncological formations). Amongst the all fluoroquinolones gemifloxacine has the best function against Borrelia with the lowest MIC and MBC.
In Vitro Activities of Fluoroquinolones against the Spirochete Borrelia burgdorferi (2001)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC90682/
4. The mechanism in which gemifloxacin works in cancer
The biological complexity of RKIP signaling in human cancers (2015)
https://www.nature.com/articles/emm201570
Gemifloxacin is a fluoroquinolone antibiotic that reportedly inhibits the migratory and invasive potential of MDA-MB-453 and MDA-MB-231 breast cancer cells. Phosphorylation of IκB and functionally active NFKB was inhibited in gemifloxacin-treated breast cancer cells.11 4-Shogaol, a phytochemical extracted from red ginger, has been shown to exert inhibitory effects on phosphorylation of IκB and NF-kB in breast cancer cells. RKIP was demonstrated to be increased in 4-Shogaol-treated breast cancer cells, and depletion of RKIP impaired 4-Shogaol-mediated biological effects. Tumor growth was also remarkably reduced in xenografted mice treated with 4-Shogaol.12 Next, we discuss how RKIP interacts with other proteins to transduce signals in cancer cells.
5. Function of Fluoroquinolones in Osteosarcoma in Canine Model.
Fluoroquinolone-mediated inhibition of cell growth, S-G2/M cell cycle arrest, and apoptosis in canine osteosarcoma cell lines (2012).https://www.ncbi.nlm.nih.gov/pubmed/22927942
„...we hypothesized that fluoroquinolone antibiotics might directly inhibit the survival and proliferation of canine osteosarcoma cells. ... These results support further studies examining the potential impact of quinolones on survival and proliferation of osteosarcoma.“
The biological complexity of RKIP signaling in human cancers (2015)
https://www.nature.com/articles/emm201570
Gemifloxacin is a fluoroquinolone antibiotic that reportedly inhibits the migratory and invasive potential of MDA-MB-453 and MDA-MB-231 breast cancer cells. Phosphorylation of IκB and functionally active NFKB was inhibited in gemifloxacin-treated breast cancer cells.11 4-Shogaol, a phytochemical extracted from red ginger, has been shown to exert inhibitory effects on phosphorylation of IκB and NF-kB in breast cancer cells. RKIP was demonstrated to be increased in 4-Shogaol-treated breast cancer cells, and depletion of RKIP impaired 4-Shogaol-mediated biological effects. Tumor growth was also remarkably reduced in xenografted mice treated with 4-Shogaol.12 Next, we discuss how RKIP interacts with other proteins to transduce signals in cancer cells.
5. Function of Fluoroquinolones in Osteosarcoma in Canine Model.
Fluoroquinolone-mediated inhibition of cell growth, S-G2/M cell cycle arrest, and apoptosis in canine osteosarcoma cell lines (2012).https://www.ncbi.nlm.nih.gov/pubmed/22927942
„...we hypothesized that fluoroquinolone antibiotics might directly inhibit the survival and proliferation of canine osteosarcoma cells. ... These results support further studies examining the potential impact of quinolones on survival and proliferation of osteosarcoma.“
III. Artemisinin and its derivatives – artemether, artesunate
Аrtemisinin is relatively low-toxic, sold as a food supplement. Its function is reinforced with a split intake (4-6 hours interval) of trivalent iron (iron without change of absorption – for example Maltofer). For example effective scheme could be: 200 mg artemisinin taken without food morning, then after 4-6 hours maltofer 1 tablet, and at evening another dose of 100 or 200 mg artemisinin. Maximal daily intake of artemisinin must not exceed 500 mg of pure artemisinin! Recommended course length – 8-14 days.
Аrtemisinin is relatively low-toxic, sold as a food supplement. Its function is reinforced with a split intake (4-6 hours interval) of trivalent iron (iron without change of absorption – for example Maltofer). For example effective scheme could be: 200 mg artemisinin taken without food morning, then after 4-6 hours maltofer 1 tablet, and at evening another dose of 100 or 200 mg artemisinin. Maximal daily intake of artemisinin must not exceed 500 mg of pure artemisinin! Recommended course length – 8-14 days.
Doctor’s best artemisinin:
https://www.iherb.com/…/doctor-s-best-best-artemisinin…/7592
NutriCology artemisinin
https://www.iherb.com/…/Nutricology-Super-Artemisinin…/3484…
Allergy Research Group - artemisinin
https://www.iherb.com/…/Allergy-Research-Group-Super…/35218…
https://www.iherb.com/…/doctor-s-best-best-artemisinin…/7592
NutriCology artemisinin
https://www.iherb.com/…/Nutricology-Super-Artemisinin…/3484…
Allergy Research Group - artemisinin
https://www.iherb.com/…/Allergy-Research-Group-Super…/35218…
Combination – Artemix (Artesunate 50mg,Artemisinin 50mg, Artemether 40mg combo)
https://www.hepalin.com/artemix.htm
Studies demonstrating the effectiveness of artemisinin in cancer
1. Use of artemisinin for treating tumors induced by oncogenic viruses and for treating viral infections (2012)https://www.google.ch/patents/US8394849…
https://www.hindawi.com/journals/bmri/2012/247597/
https://www.hepalin.com/artemix.htm
Studies demonstrating the effectiveness of artemisinin in cancer
1. Use of artemisinin for treating tumors induced by oncogenic viruses and for treating viral infections (2012)https://www.google.ch/patents/US8394849…
https://www.hindawi.com/journals/bmri/2012/247597/
2. The antiviral activities of artemisinin and artesunate (2008).https://www.ncbi.nlm.nih.gov/pubmed/18699744
Full text: https://academic.oup.com/cid/article/47/6/804/325924
Full text: https://academic.oup.com/cid/article/47/6/804/325924
3. https://selfhacked.com/blog/artemisinin/ (updated 2018)
Artemisinin Helps Prevent Cancer
In one Randomized controlled trial Artesunate combined with NP (a chemotherapy regimen of vinorelbine and cisplatin) could elevate the short-term survival rate and prolonged the TPP (time to progression) of patients with advanced non-small cell lung cancer (NSCLC) (R, R2). (2006, 2014)
Long-term treatment of two metastatic uveal melanoma patients with Artemisinin in combination with standard chemotherapy showed a significant improvement (R). (2005)
Artemether treatment was beneficial in improving the quality of life of a 75-year old male patient with pituitary macroadenoma (R). (2006)
Artemisinin and Resveratrol possessed a synergistic anti-tumor effect, this combination could be an effective therapeutic strategy for cancer (R). (2014)
ART inhibits the growth of gall bladder cell lines (via induction of ROS and cell cycle arrest) hence may be suitable for the treatment of gallbladder cancer (R1, R2). (2016, 2016)
It induced antiproliferative and proapoptotic effects in HPV-39 infected human cervical cancer cells (R). (2015)
Novel derivatives of ART (AD1-AD8) had a high antiproliferative activity against liver/colon cancer cells, further evaluation in animal models is required (R1, R2). (2013, 2016)
4. Artemisinin: against viruses, cancer and malaria (2016)
https://www.researchgate.net/…/296025973_Artemisinin_agains…
5.!!! Targeted treatment of cancer with artemisinin and artemisinin-tagged iron-carrying compounds (2005).https://www.ncbi.nlm.nih.gov/pubmed/16185154
http://www.tandfonline.com/doi/abs/10.1517/14728222.9.5.995
Artemisinin is a chemical compound that reacts with iron to form free radicals which can kill cells. Cancer cells require and uptake a large amount of iron to proliferate. They are more susceptible to the cytotoxic effect of artemisinin than normal cells.
…The authors have found that artemisinin-tagged transferrin is highly selective and potent in killing cancer cells. Thus, artemisinin and artemisinin-tagged iron-carrying compounds could be developed into powerful anticancer drugs.
6. Artemisinin as an anticancer drug: Recent advances in target profiling and mechanisms of action (2017).https://www.ncbi.nlm.nih.gov/pubmed/28643446
Full text: https://onlinelibrary.wiley.com/doi/full/10.1002/med.21446
!!! We believe these will be important topics in realizing the potential of artemisinin and its derivatives as safe and potent anticancer agents.!!!
7. Anticancer Activity of Artemisinin and its Derivatives (2017).https://www.ncbi.nlm.nih.gov/pubmed/29061778
Dihydroartemisinin and artesunate exhibit chemosensitising effects in vivo in breast, lung, pancreas and glioma cancer cells, proposing the use of ARTs also in combination anticancer therapy.
Artemisinin Helps Prevent Cancer
In one Randomized controlled trial Artesunate combined with NP (a chemotherapy regimen of vinorelbine and cisplatin) could elevate the short-term survival rate and prolonged the TPP (time to progression) of patients with advanced non-small cell lung cancer (NSCLC) (R, R2). (2006, 2014)
Long-term treatment of two metastatic uveal melanoma patients with Artemisinin in combination with standard chemotherapy showed a significant improvement (R). (2005)
Artemether treatment was beneficial in improving the quality of life of a 75-year old male patient with pituitary macroadenoma (R). (2006)
Artemisinin and Resveratrol possessed a synergistic anti-tumor effect, this combination could be an effective therapeutic strategy for cancer (R). (2014)
ART inhibits the growth of gall bladder cell lines (via induction of ROS and cell cycle arrest) hence may be suitable for the treatment of gallbladder cancer (R1, R2). (2016, 2016)
It induced antiproliferative and proapoptotic effects in HPV-39 infected human cervical cancer cells (R). (2015)
Novel derivatives of ART (AD1-AD8) had a high antiproliferative activity against liver/colon cancer cells, further evaluation in animal models is required (R1, R2). (2013, 2016)
4. Artemisinin: against viruses, cancer and malaria (2016)
https://www.researchgate.net/…/296025973_Artemisinin_agains…
5.!!! Targeted treatment of cancer with artemisinin and artemisinin-tagged iron-carrying compounds (2005).https://www.ncbi.nlm.nih.gov/pubmed/16185154
http://www.tandfonline.com/doi/abs/10.1517/14728222.9.5.995
Artemisinin is a chemical compound that reacts with iron to form free radicals which can kill cells. Cancer cells require and uptake a large amount of iron to proliferate. They are more susceptible to the cytotoxic effect of artemisinin than normal cells.
…The authors have found that artemisinin-tagged transferrin is highly selective and potent in killing cancer cells. Thus, artemisinin and artemisinin-tagged iron-carrying compounds could be developed into powerful anticancer drugs.
6. Artemisinin as an anticancer drug: Recent advances in target profiling and mechanisms of action (2017).https://www.ncbi.nlm.nih.gov/pubmed/28643446
Full text: https://onlinelibrary.wiley.com/doi/full/10.1002/med.21446
!!! We believe these will be important topics in realizing the potential of artemisinin and its derivatives as safe and potent anticancer agents.!!!
7. Anticancer Activity of Artemisinin and its Derivatives (2017).https://www.ncbi.nlm.nih.gov/pubmed/29061778
Dihydroartemisinin and artesunate exhibit chemosensitising effects in vivo in breast, lung, pancreas and glioma cancer cells, proposing the use of ARTs also in combination anticancer therapy.
8. Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug (2012, online 2011)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228295/
9. Anticancer Effect of AntiMalarial Artemisinin Compounds (2015).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389338/
…have several biological characteristics that include anticancer properties. Experimental evidences suggest that artemisinin compounds may be a therapeutic alternative in highly aggressive cancers with rapid dissemination, without developing drug resistance. They also exhibit synergism with other anticancer drugs with no increased toxicity toward normal cells. It has been found that semisynthetic artemisinin derivatives have much higher antitumor activity than their monomeric counterparts via mechanisms like apoptosis, arrest of cell cycle at G0/G1, and oxidative stress.
10. Anticancer activity of artemisinin-derived trioxanes (2006)http://www.tandfonline.com/…/a…/10.1517/13543776.16.12.1665…
Several of these new chemical entities, especially some trioxane dimers, have selective and very potent anticancer activity even at low nanomolar concentrations.!!!
9. Anticancer Effect of AntiMalarial Artemisinin Compounds (2015).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389338/
…have several biological characteristics that include anticancer properties. Experimental evidences suggest that artemisinin compounds may be a therapeutic alternative in highly aggressive cancers with rapid dissemination, without developing drug resistance. They also exhibit synergism with other anticancer drugs with no increased toxicity toward normal cells. It has been found that semisynthetic artemisinin derivatives have much higher antitumor activity than their monomeric counterparts via mechanisms like apoptosis, arrest of cell cycle at G0/G1, and oxidative stress.
10. Anticancer activity of artemisinin-derived trioxanes (2006)http://www.tandfonline.com/…/a…/10.1517/13543776.16.12.1665…
Several of these new chemical entities, especially some trioxane dimers, have selective and very potent anticancer activity even at low nanomolar concentrations.!!!
11. Anticancer properties of artemisinin derivatives and their targeted delivery by transferrin conjugation (2008).
https://www.ncbi.nlm.nih.gov/pubmed/17942255
12. Artemisinin and Its Derivatives as a Repurposing Anticancer Agent: What Else Do We Need to Do? (2016)
https://www.ncbi.nlm.nih.gov/pubmed/27739410
https://www.ncbi.nlm.nih.gov/pubmed/17942255
12. Artemisinin and Its Derivatives as a Repurposing Anticancer Agent: What Else Do We Need to Do? (2016)
https://www.ncbi.nlm.nih.gov/pubmed/27739410
13. Recent advances in artemisinin and its derivatives as antimalarial and antitumor agents (2004).
https://www.ncbi.nlm.nih.gov/pubmed/15134519
14. Artemisinin and its derivatives: a novel class of anti-malarial and anti-cancer agents (2010).
https://www.ncbi.nlm.nih.gov/pubmed/20111769
https://pubs.rsc.org/…/Con…/ArticleLanding/2010/CS/B816679J…
https://www.ncbi.nlm.nih.gov/pubmed/15134519
14. Artemisinin and its derivatives: a novel class of anti-malarial and anti-cancer agents (2010).
https://www.ncbi.nlm.nih.gov/pubmed/20111769
https://pubs.rsc.org/…/Con…/ArticleLanding/2010/CS/B816679J…
15. Medicinal chemistry perspectives of trioxanes and tetraoxanes (2011).
https://www.ncbi.nlm.nih.gov/pubmed/21824099
https://www.ncbi.nlm.nih.gov/pubmed/21824099
Бях помолен от англоезичен познат да подготвя списък на най-обещаващите в онко-терапията нискотоксични и нетоксични вещества, като акцентирам само върху най-важните статии, които лабораторно или клинично демонстрират тяхната антиракова активност. Намирам, че ще бъде полезно да публикувам писмото, тъй като темата е пряко свързана и с веществата, за които в новата микробиологична литература се открива, че имат и най-силната антиборелийна функция и са обещаващи в лечението на хроничната борелиоза. Връзките между раковите заболявания и хроничните инфекции (бактерии - особено борелиа и нейните биофилми, някои патогенни гъби, както и онковирусите) са добре установени. Ето едно добро обобщение: "Вярваме, че този биофилмен/перзистерен "посяващ (разсаждащ)" модел е валиден за различни микробни инфекции и ще има значително приложение за разработване на по-ефективни лечения на хронични (перзистиращи) инфекции и дори при РАК(!) като цяло. We believe this biofilm/persister seeding model to be valid for different microbial infections and will have broad implications for developing more effective treatments of persistent infections and even cancer in general.
биофилма структури на borrelia burgdorferi не само показват по-голяма толерантност към лаймска антибиотици, но и причиняват по-тежка патология в модел на миши артрит: последици за разбирането на упоритост, ptlds и лечение на лечението
джи фенг, тингтинг ли, ин джан.
В линк ще приложа и pdf форма на писмото.
При интерес ще се погрижа и за пълен превод на български.
скъпа...,
тук съм обобщени само три от на за ниско-токсично / не-токсично лечение на някои онкологична заболявания: тигециклин, gemifloxacin, и artemisinin и неговите производни.
през последните години на способности на флуорохинолони са били проучени внимателно. в този контекст семейството на хинолонови изглежда свързва три различни биологични дейности - антибактериални, противоракови и антивирусни профили, а прегледът може също така да даде възможност за прозрение на различните механизми, отговорни за тези дейности сред различни видове. като четвърто поколение флуороквинолон, gemifloxacin се различава от други не само в ниската си токсичност, но и в относително редки случаи (ако има такива) от нежелани реакции. прилагането на artemisinin е много практично, тъй като сега е на разположение като хранителна добавка. през последните 30 години неговата противоракови, антивирусна, противогъбични, антипаразитни и антималарийни функция е била добре доказана. по-специално, при онкологична прояви и тумори, причинени от oncoviruses, неговата селективна апоптозис функция срещу раковите клетки се увеличава значително с разделим прием на тривалентна желязо (минимум 4 часа интервал в на прием на artemisinin и желязо).
във второ писмо ще ви предоставя информация за на функция и прилагане на други за вещества като мощните атф инхибитори - disulphiram и gambogic киселина. що се отнася до тях, вече има някои успешни клинични резултати, като и двете са включени в на протокол за лечение на най-агресивната форма на мозъчен тумор - глиобластома. други възможности за нетоксични лечение с рак са също някои съединения с селективна цитотоксичност като тамян и смирна етерични масла (и им им комбинация), карвакрол (от риган основни масло), цинамалдехид (от основни основни масло), чесън основни масло, което може да бъде подготвено в на форма за по-добра доставка. (билкова медицина: биомолекулярни и клинични аспекти. 2-ро издание. 2011. глава 17. билки и подправки при профилактика и лечение на рак.https://www.ncbi.nlm.nih.gov/books/NBK92774/).
особено важно в тази област са някои от на и цефалоспорини група антибиотици - cefoperazone + sulbactam, azlocillin, цефтриаксон, пиперацилин-тазобактам и др. не е изненадващо всички тези съединения (включително етерични масла, но с по-добра доставка за in vivo приложение, защото имат много ниска бионаличност при хората!) имат най-силната antiborrelial активност и са много обещаващи в лечението на постоянни форми на borreliosis - хронично лаймска болест да. връзката между ракови заболявания и бактерии (особено borrelia и техните биофилми), някои патогенни гъбички (онкогенни гъбички) и oncoviruses е добре установена.
то е добре обобщено и apodictically доказано в неотдавнашно проучване (https://www.biorxiv.org/content/early/2018/10/13/440461): " вярваме, че този биофилма / persister засяване модел е валиден за различни микробен инфекции и ще има широки последици за разработването на по-ефективни лечения на трайни инфекции и дори рак като цяло."
искрено твой,
Yanko Marinov (23. 02. 2019)
ниско-токсични / не-токсични противоракови съединения.
първа част: аз. тигециклин. - да. gemifloxacin. iii. artemisinin и производни
аз аз тигециклин
1. на лекарство тигециклин: фокус върху неговите обещаващи противоракови свойства (2016)
целта на този преглед е да се обобщи на анти-тумор доказателства, подкрепящи активността на тиг срещу различни видове рак, включително остра миелоидна левкемия (омл), глиом, не-малък рак на белия дроб (ндкрбд), наред с други. освен това ефикасността и нежеланите реакции на тиг при пациенти с рак са обобщени подробно. трябва да се обсъдят и бъдещи клинични проучвания, които ще оценят сигурността и ще потвърдят основните свойства, свързани с тумора на тиг.
2. тигециклин инхибира растежа на глиом чрез регулиране на мирна-199 b-5 p-hes1-akt път. (2016)
3. насочване на митохондриална оксидативен фосфорилиране премахва терапия-резистентни хронична стволови клетки (2017)https://www.nature.com/articles/nm.4399
тигециклин може селективно да се насочи към стволови клетки от левкемия при хмл (2017)
основна находка: тигециклин инхибира митохондриална оксидативен фосфорилиране към целта стволови клетки на левкемия (lsc).
концепция: тигециклин цели cd34+cd38− клетки на хмл с малък ефект върху nonleukemic cd34+cd38− клетки.
въздействие: иматиниб плюс тигециклин може да се насочи към lscs и диференцирани клетки на хмл за потискане на рецидив на хмл
4. терапевтично взаимодействие между тигециклин и venetoclax в предклинични модели на гъ / bcl2 двойно-хит b клетъчен лимфом. (2018)
авторите са открили, че чифт клинично одобрени лекарства са показали взаимодействие срещу рака и също така са били ефективни в комбинация с ритуксимаб, което е основата на текущото лечение за лимфома.
5. резултати от на, контролирано, рандомизирано клинично проучване, което оценява комбинацията от пиперацилин / тазобактам и тигециклин при пациенти с висок риск при пациенти с рак с фебрилна неутропения.
заключение: комбинацията от пиперацилин / тазобактам и тигециклин е безопасна, добре поносима, и по-ефективна от пиперацилин / тазобактам самостоятелно при фебрилна, висок риск, неутропения хематологични пациенти с рак. в епидемиологични настройки, характеризиращи се с високо разпространение на инфекции поради mdr микроорганизми, тази комбинация може да се счита за една от първите линия антибиотик терапии. http://ascopubs.org/doi/full/10.1200/JCO.2013.51.6963
6. добавянето на тигециклин към емпирично терапия подобрява степента на успех при пациенти с фебрилна неутропения с хематологични злокачествени заболявания (2014)http://www.ascopost.com/News/16145
7. инхибиране на митохондриална превод като терапевтична стратегия за човешка остра миелоидна левкемия. (2011) тигециклин селективно е убил стволови клетки и стволови клетки в сравнение с техните нормални колеги и също така е показал antileukemic активност при миши модели на човешка левкемия. shrna-медиирани нокдаун на ef-ту митохондриална коефициент на превод в левкемия клетки възпроизвежда на активност на тигециклин. тези ефекти са били производни на митохондриална биогенеза, че заедно с повишена basal консумация на кислород се оказва, че се повишава при омл спрямо нормалните хемопоетични клетки и също така са били важни за тяхната разлика в чувствителността на тигециклин.
употреба на тигециклин при пациенти с рак със сериозни инфекции: доклад за 110 случая от една институция. (2009)
9. фаза 1 проучване на интравенозни инфузии на тигециклин при пациенти с остра миелоидна левкемия (2016).
tg се прилага над седем нива на доза (50-350 mg / ден). двама пациенти са имали dlts, свързани с тигециклин на ниво 350 mg / дневно, което води до максимална поносима доза тигециклин от 300 mg като веднъж дневно инфузия. фармакокинетичните експерименти показват, че тигециклин е имал значително по-кратък полуживот при тези пациенти, отколкото при пациенти с noncancer. не са наблюдавани значими фармакодинамични промени или клинични реакции. по този начин ние сме определили безопасността на веднъж дневно тигециклин при пациенти с огнеупорни миелоидна левкемия. бъдещите проучвания трябва да се фокусират върху графиците на лекарството, което позволява по-устойчиво потискане на целта.
- да. gemifloxacin
няколко статии за функцията за инхибиране на растежа на раковите клетки и метастази. gemifloxacin (factive) имат добра бионаличност, вътреклетъчни и проникване в цнс.
1. gemifloxacin, на антимикробни лекарство, инхибира миграцията и нахлуването на ракови клетки от човешки дебелото черво (2013)
пълен текст: https://www.hindawi.com/journals/bmri/2013/159786/
" в заключение, гмф може да е нов противоракови агент за лечение на метастази в рак на дебелото черво."!!!
2. gemifloxacin инхибира миграцията и инвазията и индуцира мезенхимните-епителни преход в клетки за аденокарцином на човешки гърди (2013)
пълен текст:
" това проучване показва, че гмф може да бъде нов противоракови агент за профилактика и лечение на метастази при рак на гърдата. гмф инхибира миграцията и нахлуването в клетките на човешки на човешки гърди. гмф индуцира тдпи чрез намаляване на nf-kb и активирането на охлюви и чрез увеличаване на нивата на rkip. гмф има потенциално клинично отражение като анти-метастатичен агент за рак на гърдата. " " "
3. проучване (in vitro) за gemifloxacin функция в borrelia (което често е причина за онкологична формации). сред всички флуорохинолони gemifloxacine има най-добрата функция срещу borrelia с най-ниския микрофон и метастазирал рак на млечната жлеза.
in vitro дейности на флуорохинолони срещу на borrelia burgdorferi (2001)
4. механизмът, в който gemifloxacin работи в рак
биологичната сложност на rkip сигнали при човешки рак (2015)
gemifloxacin е флуороквинолон антибиотик, който според съобщенията инхибира на и инвазивни потенциал на mda-мб-453 и mda-mb-231 клетки за рак на гърдата. доказано е, че фосфорилиране на ikb и функционално активен nfkb е инхибира в gemifloxacin-третирани клетки от рак на гърдата. 11 4-shogaol, на, извлечен от червен джинджифил, е доказано, че оказва инхибиторна ефект върху фосфорилиране на ikb и nf-kb в ракови клетки. доказано е, че rkip се увеличава при 4-shogaol клетки от рак на гърдата и изчерпване на rkip 4-shogaol-медиирани биологични ефекти. растежът на тумора също е бил значително намален при xenografted мишки, лекувани с 4-shogaol. 12 след това обсъждаме как rkip взаимодейства с други протеини, за да transduce сигнали в раковите клетки.
5. функция на флуорохинолони в остеосаркома в кучешки модел.
флуороквинолон-медиирани инхибиране на клетъчния растеж, s-g2 / m цикъл на клетъчния цикъл, и апоптоза в кучешки остеосаркома клетъчни линии (2012). https://www.ncbi.nlm.nih.gov/pubmed/22927942
"... смятахме, че флуороквинолон антибиотици могат директно да инхибират оцеляването и разпространението на кучешки остеосаркома клетки. ... тези резултати подкрепят по-нататъшни проучвания, които разглеждат потенциалното въздействие на хинолони върху оцеляването и разпространението на остеосаркома."
iii. artemisinin и неговите производни - artemether, artesunate
аrtemisinin е относително ниско-токсичен, продаден като хранителна добавка. функцията му е подсилена с разделим прием (4-6 часа интервал) от тривалентна желязо (желязо без промяна на абсорбцията - например maltofer). например ефективна схема може да бъде: 200 mg artemisinin, взети без храна сутрин, след това след 4-6 часа maltofer 1 таблетка, а вечер друга доза от 100 или 200 mg artemisinin. максималният дневен прием на artemisinin не трябва да надвишава 500 mg чист artemisinin! препоръчителна дължина на курса-8-14 дни.
най-добрият artemisinin на доктора:
nutricology artemisinin
група за изследване на алергиите - artemisinin
комбинация - artemix (artesunate 50 mg, artemisinin 50 mg, artemether 40 mg комбинация)
проучвания, показващи ефективността на artemisinin при рак
1. употреба на artemisinin за лечение на тумори, предизвикани от онкогенни вируси и за лечение на вирусни инфекции (2012)https://www.google.ch/patents/US8394849?utm_source=gb-gplus-sharePatent
2. на дейности на artemisinin и artesunate (2008).https://www.ncbi.nlm.nih.gov/pubmed/18699744
пълен текст: https://academic.oup.com/cid/article/47/6/804/325924
3. https://selfhacked.com/blog/artemisinin/ (актуализиран 2018)
artemisinin помага за предотвратяване на рак
при едно рандомизирано контролирано проучване, съчетано с нп (схема на химиотерапия на винорелбин и цисплатин), може да се повиши скоростта на преживяемост и да се удължи на (време до прогресия) на пациенти с напреднал за рак на белия дроб (ндкрбд) (р) (р) ( , r2. (2006, 2014)
дългосрочно лечение на две метастазирал uveal меланома пациенти с artemisinin в комбинация със стандартна химиотерапия показва значително подобрение (r). (2005)
лечението с artemether е полезно за подобряване на качеството на живот на 75-годишен мъжки пациент с хипофизата macroadenoma (r). (2006)
artemisinin и ресвератрол са притежавали синергични анти ефект, тази комбинация може да бъде ефективна терапевтична стратегия за рак (r). (2014)
изкуството инхибира растежа на клетъчните линии на жлъчния мехур (чрез индукция на ареста на рос и клетъчния цикъл), следователно може да бъде подходящ за лечение на рак на жлъчния мехур (r1, r2). (2016, 2016)
той предизвиква антипролиферативни и proapoptotic ефекти при hpv-39 инфектирани човешки цервикална клетки (r). (2015)
новите производни на изкуството (add1-a D8) са имали висока антипролиферативни активност срещу раковите клетки на черния дроб / дебелото черво, се изисква допълнителна оценка при модели на животни (r1, r2). (2013, 2016)
4. artemisinin: срещу вируси, рак и малария (2016)
5.!!! целенасочено лечение на рак с artemisinin и artemisinin-отбелязани съединения на желязо (2005).https://www.ncbi.nlm.nih.gov/pubmed/16185154
artemisinin е химично съединение, което реагира с желязо, за да се образуват свободни радикали, които могат да убиват клетки. раковите клетки изискват и използват голямо количество желязо, за да се размножават. те са по-податливи на на ефект на artemisinin, отколкото на нормалните клетки.
... авторите са открили, че artemisinin-отбелязани трансферин е силно селективен и мощен в убиването на ракови клетки. по този начин artemisinin и artemisinin съединения съединения могат да бъдат разработени в мощни противоракови лекарства.
6. artemisinin като противоракови лекарство: скорошен напредък в целевите профили и механизми на действие (2017).https://www.ncbi.nlm.nih.gov/pubmed/28643446
!!! смятаме, че това ще бъдат важни теми за реализиране на потенциала на artemisinin и неговите производни като безопасни и мощни противоракови агенти.!!!
7. противоракови активност на artemisinin и неговите производни (2017). https://www.ncbi.nlm.nih.gov/pubmed/29061778
dihydroartemisinin и artesunate показват chemosensitising ефекти in vivo при рак на гърдата, белия дроб, панкреаса и глиом, като предлагат използването на изкуства и в комбинация противоракови терапия.
8. antitumor активност на artemisinin и неговите производни: от добре познат антималарийни агент до потенциално противоракови лекарство (2012, онлайн 2011)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228295/
9. противоракови ефект на антималарийни artemisinin съединения (2015).
... има няколко биологични характеристики, които включват противоракови свойства. експерименталните доказателства показват, че artemisinin съединения могат да бъдат терапевтична алтернатива при силно агресивни ракови заболявания с бързо разпространение, без да се развива резистентност към наркотици. те също така показват синергизма с други противоракови лекарства без повишена токсичност към нормалните клетки. установено е, че полусинтетичен artemisinin производни имат много по-висока antitumor активност от им си колеги чрез механизми като апоптоза, арест на клетъчния цикъл при г0 / g1, и оксидативен стрес.
10. противоракови активност на artemisinin-производни trioxanes (2006)http://www.tandfonline.com/doi/abs/10.1517/13543776.16.12.1665?journalCode=ietp20
няколко от тези нови химически образувания, особено някои trioxane димери, имат избирателна и много мощна противоракови активност дори и при ниски наномол концентрации.!!!
11. противоракови свойства на artemisinin производни и тяхната целева доставка от трансферин конюгация (2008).
12. artemisinin и неговите производни като на противоракови агент: какво друго трябва да направим? (2016)
13. скорошни авансови постижения в artemisinin и неговите производни като антималарийни и antitumor агенти (2004).
14. artemisinin и неговите производни: нов клас анти-маларична и анти-ракови агенти (2010).
15. 15. 15. лекарствени гледни точки на trioxanes и tetraoxanes (2011).
Няма коментари:
Публикуване на коментар