At this point we are thinking about trying 1 mg of daily Rapamycin to slow the cancer cell growth plus the DAV therapy. If he can live several months longer, we’ll count it as a win. I think it’s not possible to cure it at this point. Thoughts?
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Like previously posted here in this thread, it could slow down the cancer. But I don’t know at what dose.
“mammilian target of rapamycin (mTOR) is a very important serine/threonine protein kinase involved in the regulation of energy metabolism, cell growth, angiogenesis and other cellular biological processes.Rapamycin (sirolimus) is a selective inhibitor of mTOR kinase, which can inhibit the activation and proliferation of T lymphocytes to inhibit the immune response.Currently, mTOR inhibitors are also widely used in tumor treatment. Several studies have been performed to evaluate the efficacy of sirolimus in some solid tumors, and encouraging results are obtained. However, the existing studies on mTOR inhibitors and pancreatic cancer treatment are mostly phase I trials, with little evaluation of the efficacy. Therefore, the phase II clinical trial of rapamycin in the treatment of pancreatic cancer is very necessary.”
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Would 1 mg of Rapamycin a day be enough? 2 mg? A big dose weekly? There’s nothing to lose, but I would like to take the most optimal bet.
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If it were me I’d take it daily but start at 1mg for a few weeks and then see if any effects. If not then try 2g and again then see if any effects. If not then try the other end of the scale with 12-14mg fortnightly or 30mg once every four weeks. Again then see if any effects. Hopefully one of those shows at least a halt in progression which buys you time to try other things.
Keeping my fingers crossed for you - good luck!!
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Does anyone know how much Rapamycin Dr. Blagosklonny is taking? I would like to give the same regimen to my father in law for his cancer. Thank you.
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Thanks for the wonderful responses in other threads.
Dr. Sehgal took 1 mg of Rapamycin daily.
Cancer patients take about 10 mg Everolimus daily which translates to about 5 mg Sirolimus daily.
We may go with 6 mg equivalent or 2 mg + GFJ daily.
We will probably need 1-2 rest days each week. How many should he do?
Thoughts on this proposed protocol?
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Can anyone comment on doing the DAV therapy (Doxycycline Azithromycin Vitamin C) and Rapamycin at the same time. Is it a good idea or not? Thanks for any input.
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I am sorry for your problems. You are certainly a good and kind son-in-law.
I have done the DAV therapy twice. Once I stopped taking rapamycin the second time I was on my regular 1/week schedule. I had zero side effects or any subjective effects which I assume is because I don’t have any known cancer.
If I were to advise anyone, and I wouldn’t want to, who had a cancer problem that wasn’t being helped by conventional methods, I would take Dr. Blagosklonny’s advocacy and take the highest tolerable dose of rapamycin. His opinion papers indicate that he believes it is a cancer treatment.
As for the DAV treatment, I would follow the regimen advocated by Joseph.
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It seems that Sirolimus (Rapamycin) can be effective at weakening cancer on its own. However, when a traditional chemotherapy is added, the effects are even greater. I wish we hadused Rapamycin in addition to chemo in the first place!
After consulting with the hospital, we are considering the last chemotherapy that they have available, TS-1 combined with Sirolimus. TS-1 converts to 5-Fluorouracil in the body. Unfortunately, the cancer may already be resistant to it as it was used in another treatment already. Still, we hope that the addition of Sirolimus will make the drug effective again. If so, then this could open up the door to trying other chemo drugs already used paired with Sirolimus to extend lifespan.
In the early-treatment experiment, the tumor growth rate was inhibited by 48% in the group treated by rapamycin alone, by 34% in the 5-fluorouracil-treated group, and by 60% in the group treated with rapamycin plus 5-fluorouracil compared to the control mice
There are already precedents set for Gemcitabine resistant cancers, such as adding Sirolimus, where the resistant cancers are affected by Gemcitabine more than non-resistant cancers due to the Sirolimus.
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Perhaps consider
Our clinical trials looking into Fast-Mimicking Diet (FMD) and cancer prevention and treatment are ongoing. But if early results are any indication, it could be a powerful new weapon in the arsenal we have to fight, and one day defeat, cancer.
Papers etc here Cancer - Valter Longo can also check the latest clinical trials
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Update: Father in law took his fast acting insulin and then forgot to eat, so it’s probably not the Rapamycins fault for the hypoglycemia.
Found this other comment by John Hemming citing research that sodium citrate (+ other citrates) can potentiate both chemotherapy and Rapamycin in the treatment of cancer : A concern about senolytics not supported by mouse studies - #7 by John_Hemming
This may be related to the alternate medicine Alkaline Approach mentioned by Viktor above. Sodium citrate (balanced with other citrates, like potassium and magnesium citrates and taken in several doses over the day to avoid electrolyte imbalances) does indeed Alkalinize many tissues including cancer tissues. John Hemming has reported that his Urine has a PH of 9 or 10! The oral dosage in mice that was effective for cancer is 500mg/kg/day, not clear how that scales to humans.
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This is the mass vs square meters of skin question. Obviously for a 80kg human if that scales it would be 40g. I tend to measure the mass of citrate which is perhaps 2/3 of the citrate salt (it varies depending on the cation). There is an additional complication that the different salts have a tendency to have a bit of water with them as well.
There is an interesting question as to whether the alkanisation of the tissues is itself positive separate to the provision of citrate.
Blood transfusions tend to come with a large dose of sodium citrate as well.
As an alternative scaling
https://www.publish.csiro.au/bi/pdf/bi9670687#:~:text=From%20Figure%201%20the%20surface,2-90·4%20cm2%20.
From Figure 1 the surface area of a mouse weighing 25·7 g is estimated to be 78·6 cm2 , with a range (95% confidence limits) of 68·2-90·4 cm2 .
So lets say the mouse is 25g which means a dose of 500mg*0.025= 12.5mg
Using the figure of 1.6square metres for humans and 80square centimetres (80/10000 square meters) the ratio would be 200 which gives a dose of 2.5g.
I think 2.5g is very low.
Alternatively mice eat about 5g a day and humans perhaps 1.2kg which is a ratio of 240.
That fits closer to the skin ratio. The mass ratio is 3,200.
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correction: you mean obviously 12.5mg
You are right about this. I will fix the post.
Another peptide worth looking into regarding cancer is PNC 27. And specially for pancreatic cancer:
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Good call. It’s called safeguard for good reason, not much downside. My daughter has been on high dose for a long time and she just got scanned a couple days ago, no evidence of disease.
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Since we are talking about last-ditch efforts, I might add this paper reviewing different peptides which may fight cancers. I have no firsthand knowledge of these but the paper came up in something else I was reading (PNC-27 out of pure interest as someone who had cancer and is intrigued by peptides and their possibilities). Maybe there are some possibilities for your family they may be synergistic (or not obstructive) to what you are already trying.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5359827/
In the paper they mention specifically for pancreatic cancers:
| PNC-2 and PNC-7 | in vitro | Pancreatic cancer (MIA-PaCa) cells | [109] |
|---|
|Cardiac natriuretic peptides|In vitro & in vivo|Pancreatic cancer (HPAC), renal carcinoma (SW156), breast adenocarcinoma (HCCI428), ovarian adenocarcinoma (NIHOVCAR-3), modularly thyroid carcinoma (TT), glioblastoma (LNZTA3WT4) and lung carcinoma (NCI-H1963) cells|
p16 In vitro Pancreatic cancer (AsPC-1 and BxPC-3) cells [166]
PNC-27 In vitro Cervical carcinoma (HeLa), colon cancer (SW1417 and H11299), breast cancer (MDA-MB-453 and MCF-7), osteosarcoma (SAOS2), leukaemia (K562), pancreatic cancer (MIA-PaCa-2) and melanoma (A-2058) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214, 216, 217]
PNC-21 In vitro Cervical carcinoma (HeLa), colon cancer (SW1417 and H1299), breast cancer (MDA-MB-453), and osteosarcoma (SAOS2) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214]
PNC-28 In vitro & in vivo Breast cancer (MDA-MB-453), colon cancer (H1299 and SW1417), osteosarcoma (SAOS2), cervical carcinoma (HeLa) and pancreatic cancer (MiaPaCa-2) cells. Rat k-ras-transformed pancreatic cancer (TUC-3) and transformed endothelial (E49) cells [214, 219,
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You have my sympathy.
IMO: I would certainly not pursue alternative medicine or other unproven therapies at the beginning of discovering cancer. But, once it reaches stage four and the doctor’s therapy is not stopping or curing the cancer, all bets are off.
What have you got to lose by trying any alternative solutions?
My wife died from the complications of breast cancer. I am so sorry I did not intervene with the doctors’ therapies when it continued to progress.
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Nanoparticle delivery of innate immune agonists combined with senescence-inducing agents promotes T cell control of pancreatic cancer
New combination therapy approach for pancreatic cancer.
https://www.science.org/doi/10.1126/scitranslmed.adj9366
Unlike other tumor types, existing immunotherapies have not proven very successful for pancreatic ductal adenocarcinoma (PDAC), necessitating the development of additional approaches. Here, Chibaya et al. developed a combination therapy approach that included nanoparticle delivery of STING and TLR4 agonists, which stimulate the immune response, in combination with the MEK inhibitor trametinib and CDK4/6 inhibitor palbociclib, which promote senescence of tumor cells. The combination therapy induced robust antitumor immune responses that controlled tumor burden in implanted and autochthonous PDAC mouse models. These data support further development of this potent combination therapy for PDAC.
Pancreatic ductal adenocarcinoma (PDAC) has quickly risen to become the third leading cause of cancer-related death in the United States. This is in part because of its fibrotic tumor microenvironment (TME) that contributes to poor vascularization and immune infiltration and subsequent chemo- and immunotherapy failure. Here, we investigated an immunotherapy approach combining delivery of stimulator of interferon genes (STING) and Toll-like receptor 4 (TLR4) innate immune agonists by lipid-based nanoparticle (NP) coencapsulation with senescence-inducing RAS-targeted therapies, which can remodel the immune suppressive PDAC TME through the senescence-associated secretory phenotype.This two-pronged approach produced potent T cell–driven and type I interferon–mediated tumor regression and long-term survival in preclinical PDAC models dependent on both tumor and host STING activation.
Collectively, our results suggest that engineering approaches to target multiple cell types and immune suppressive barriers through induction of type I IFN signaling in the PDAC TME could pave the way for coordinated innate and adaptive immune responses to achieve immunotherapy successes that have thus far been elusive for patients with PDAC.
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