Prostate Cancer

This post is intended to be a part of the “Cancer Type” category, and represents a list of info including drugs and supplements that may be relevant when fighting prostate cancer. Note that these drugs and supplements must not represent the replacement of conventional therapies. Instead, they may be used in agreement with the medical doctor to increase the chance of success of current therapies or represent additional options when conventional treatments are not available anymore. Based on the references below, here are the drugs and supplements I would consider:

  1. Metformin (typical dose: 1000mg to 2000mg/day)
  2. Atorvastatin (typical dose: see drug info)
  3. Aspirin (or Celecoxib) (typical dose: 100mg/day)
  4. Vitamin D3 (typically taken at about 5000ui to 10.000ui/day by cancer patients) D3 blood level needs to be monitored from time to time. Here is an example of a home test kit to do that
  5. Zinc + Chloroquine or Disulfiram
  6. Xanthohumol
  7. Pyrvinium pamoate (typical dose: see  previous post)
  8. Vitamin C and Vitamin K3 and Vitamin E
  9. Lycopene
  10. HCA+ALA (see below why and read more about this route here)
  11. Baicalein

Although not intended, some of the above are also part of the Anti cholesterol strategy I put together sometime ago: Due to the hormonal connection of prostate cancer, and since cholesterol represents the fuel for hormone production, I believe the anti cholesterol strategy is very relevant in prostate cancer.

Update on 27 Sept 2017: Supporting my expectation stated above, recently, a prostate cancer patient reported on this website response to HCA+Alpha Lipoic Acid (lasting for about 2 years) (Ref.). HCA is indeed an important elements in the Anti-cholesterol strategy, that I expect to be relevant to prostate cancer.

This list will further updated during the coming days/weeks.


Metformin is widely accessible at pharmacies around the world, is cheap and it is typical used at a dose of 500mg to 2000mg/kg. In general, I would go for 1000mg to 1500mg/day. I would start with 500mg/day and increase the daily dose each week with 250mg towards the target dose.

Molecular pathways and targets in prostate cancer  “A recent population study performed in Toronto showed that increasing duration of metformin use among diabetic men after a diagnosis of prostate cancer was associated with decreased prostate cancer–specific and all-cause mortality [347]. The findings were significant irrespective of what treatments the subjects were receiving for their PCa. Metformin is a widely used drug to treat type II diabetes, and is currently explored in numerous types of cancer, including PCa, in about 10 trials. In particular, addition of metformin to various forms of ADT is explored based on the rationale that ADT is associated with the metabolic syndrome, hyperinsulinemia and insulin resistance. Hyperinsulinemia was reported to stimulate tumor growth and development of CRPC via activation of IGFR. Metformin through its activation of the AMPK-LKBI pathway reduces liver gluconeogenesis secondarily decreasing insulin levels, which might explain the effects on tumor growth. Other effects of metformin on cellular metabolic processes could contribute to its anti-cancer properties, such as indirect effects on mTOR and SIRT1. Metformin acts directly on mitochondrial complex I reducing respiration rates, and this activity is probably relevant to the recently demonstrated improvement of prostate tumors oxygenation and radiotherapy response in vivo [348]. Metformin use was associated with significant decrease in biochemical relapse in patients [348].”

Metformin sensitizes prostate cancer cells to radiation through EGFR/p-DNA-PKCS in vitro and in vivo.  Our results indicate that metformin enhances prostate cancer cell radiosensitivity in vitro and in vivo. Exposure to metformin before radiation therapy could be a beneficial option for the treatment of prostate cancer.

Metformin and Prostate Cancer: a New Role for an Old Drug  Overall available data support the potential dual benefit of metformin on ADT-induced metabolic syndrome and in its antineoplastic activity in prostate cancer, justifying the need for ongoing clinical trials to confirm these effects as the evidence currently available for standard practice is lacking.

A prospective, randomized pilot study evaluating the effects of metformin and lifestyle intervention on patients with prostate cancer receiving androgen deprivation therapy. The present study shows the potential benefits of metformin and lifestyle changes in ADT-treated men. Further studies will aim to determine which intervention is most important, and may show that overall survival can be improved.

Mechanistic Study of Inhibitory Effects of Metformin and Atorvastatin in Combination on Prostate Cancer Cells in Vitro and in Vivo. Results of the present study indicate the combination of metforminand atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.

Atorvastatin (and other statins)

Combined effects of atorvastatin and aspirin on growth and apoptosis in human prostate cancercells. The findings provide a strong rationale for clinical evaluation of the combination of atorvastatin and aspirin in patients with prostate cancer.

Mechanistic Study of Inhibitory Effects of Metformin and Atorvastatin in Combination on Prostate Cancer Cells in Vitro and in Vivo Results of the present study indicate the combination of metforminand atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.

A phase II study of atorvastatin and celecoxib in patients with rising PSA following local therapy for prostate cancer (PC) In this ongoing phase II trial, the combination of low dose atorvastatin and celecoxib has been well tolerated and demonstrates a tendency of increasing PSA doubling time. Enrollment continues with analysis of IL-6, CRP, and PGE-2 to be correlated to individual clinical results.

The differential effects of statins on the metastatic behaviour of prostate cancer. Lipophilic statins reduce the migration and colony formation of PC-3 cells in human BMS by inhibiting GGPP production, reducing the formation and the spread of metastatic prostate colonies.

Statins, especially atorvastatin, may improve survival following brachytherapy for clinically localized prostate cancer. The patients taking statin medications had significantly lower prostate-specific antigen values, percent positive biopsies, and prostate volume than those patients not taking statin medications. Statin usage resulted in a nonstatistical improvement in all survival parameters with the results most pronounced for atorvastatin.

Statin Use in Prostate Cancer: An Update Although still premature, accumulating clinical evidence suggests that statin use may be beneficial in the prevention and/or treatment of prostate cancer.


Regular Aspirin Use and the Risk of Lethal Prostate Cancer in the Physicians’ Health Study. Current regular aspirin use was associated with a lower risk of lethal PC among all participants. Current postdiagnostic use was associated with improved survival after diagnosis, consistent with a potential inhibitory effect of aspirin on PC progression. A randomized trial is warranted to confirm or refute these findings.

Aspirin Use Reduces the Risk of Aggressive Prostate Cancer and Disease Recurrence in African-American Men. Regular aspirin use before and after a prostate cancer diagnosis may prevent the development of aggressive disease in AA men who are at risk of a lethal malignancy

Prostate Cancer and Aspirin Use: Synopsis of the Proposed Molecular Mechanisms. Aspirin, a non-steroidal anti-inflammatory drug (NSAID), affects the proliferation, apoptosis, resistance and metastasis of PCa cell lines, through both COX-dependent and COX-independent mechanisms. It also lowers levels of the PCa diagnostic marker prostatespecific antigen (PSA)

Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. However, aspirin use both before and after prostate cancer diagnosis was associated with longer overall survival, highlighting the importance of comorbidity prevention among prostate cancer survivors.

Aspirin may help men with prostate cancer live longer, study suggests

Vitamin D3

Vitamin D Receptor Protein Expression in Tumor Tissue and Prostate Cancer Progression High VDR expression in prostate tumors is associated with a reduced risk of lethal cancer, suggesting a role of the vitamin D pathway in prostate cancer progression.

Associations of Circulating 25-hydroxyvitamin D with prostate cancer diagnosis, stage and grade Our study provides evidence that lower 25(OH)D concentrations were associated with more aggressive cancers

Vitamin D Deficiency Predicts Prostate Biopsy Outcomes In AA men, vitamin D deficiency was associated with increased odds of PCa diagnosis on biopsy. In both EA and AA men, severe deficiency was positively associated with higher Gleason grade and tumor stage.

Molecular pathways mediating the anti-inflammatory effects of calcitriol: implications for prostate cancer chemoprevention and treatment. Calcitriol or its analogs may have utility as chemopreventive agents and should be evaluated in clinical trials in PCa patients with early or precancerous disease.

Mechanisms of vitamin D-mediated growth inhibition in prostate cancer cells: inhibition of the prostaglandin pathway. We postulate that the regulation of the PG pathway contributes to the growth inhibitory actions of calcitriol. We also propose that calcitriol can be combined with non-steroidal anti-inflammatory drugs (NSAIDs) that inhibit COX enzyme activity, as a potential therapeutic strategy in PCa.

Zinc & Zinc Ionophores

Role of zinc in the pathogenesis and treatment of prostate cancer: critical issues to resolve  Prostate malignancy involves the metabolic transformation of normal zinc-accumulating citrate-producing cells to citrate-oxidizing malignant cells that have lost the ability to accumulate zinc. Malignant cells in PCa virtually never contain high zinc levels. The lost ability to accumulate zinc is an essential metabolic transformation that is required for the manifestation of the malignant activities of the neoplastic malignant prostate cell. Downregulation of ZIP (zinc uptake) transporter gene expression might be responsible for the lost ability to accumulate zinc; and, therefore, could be a significant genetic factor in PCa.

According to the article above we need to find a way to enhance the zinc uptake into the cells.

Here there is a paper indicating that Chloroquine drug (previously discussed on this website) acts as a Zinc ionophore and has the potential to increase the cellular Zink uptake:

Chloroquine Is a Zinc Ionophore Chloroquine enhanced zinc uptake by A2780 cells in a concentration-dependent manner, as assayed using a fluorescent zinc probe.

According to the article above Clioquinol drug (available at the pharmacy) seems to also be able to do a similar job, i.e. transport Zinc inside the cell. Here is their previous article demonstrating that

Yet another approach may be to combine Disulfiram with Zinc, as Disulfiram seems to be a Zn ionophore as well. The drawback is that the patient will not be able to drink any amount of alcohol when using Disulfiram (an antialcohol drug). The dosage for  Disulfiram and Zn can be found in the following patent:

Here is a recent PhD thesis discussing the combination of Disulfiram and Zn in breast cancer as an anticancer approach: Investigation into the effects of zinc on the anti-breast cancer properties of disulfiram also stating the following: “The low concentrations of either copper and zinc required to increase disulfiram potency, suggest that increasing the availability of either metal ion could be achievable in vivo with oral supplements to enhance the cytotoxic effects of the drug.”

Therefore this trick may be relevant to other cancers. Indeed, it is well known that some tumors (like breast cancer) accumulate higher level of Zinc compared to normal cells. Even more, the higher the Zinc level in those tumors the more aggressive they are. However, the PhD thesis above demonstrates that these tumors have their own way to balance that high level of Zinc, and when that is disrupted and more Zinc is pushed into the cell (using Zinc inophores such as Disulfiram) they will be killed.

Note that Chloroquine is a base (from a chemical point of view) and it may not cross the acidity area around some tumors. This means that “alkalizing” the tumor environment during the Zinc + Chloroquine usage may help. “Alkalizing” may be done with e.g. proton pump inhibitors like Omeprazole (an over the counter drug) or possibly with Sodium Bicarbonate (I would prefer the first approach).


Xanthohumol, a natural extract that can be found online as a supplement (e.g. here), prevents the receptor from translocating to the cell nucleus, thus inhibiting its potential to stimulate the secretion of PSA and other hormone-dependent effects (Ref.)

Why beer is the latest hope in fight against cancer (Ref.) Researchers at the German Cancer Research Centre in Heidelberg have discovered that beer contains a powerful molecule that helps protect against breast and prostate cancers.

Xanthohumol impairs human prostate cancer cell growth and invasion and diminishes the incidence and progression of advanced tumors in TRAMP mice. The ability of XN to inhibit prostate cancer in vitro and in vivo suggests that XN may be a novel agent for the management of prostate cancer.

Growth Inhibitory and Apoptosis-inducing Effects of Xanthohumol, a Prenylated Chalcone Present in Hops, in Human Prostate Cancer Cells Induction of apoptosis by XN was associated with the inhibition of prosurvival Akt, NF-κB and mTOR signaling proteins and NF-κB-regulated anti-apoptotic Bcl-2 and survivin. These studies provide a rationale for clinical evaluation of XN for the treatment of hormone-refractory metastatic prostate cancer.

Pyrvinium pamoate

I already discussed this drug in details here

New medication treats drug-resistant prostate cancer in the laboratory

The novel role of pyrvinium in cancer therapy. The overwhelming insights into the mechanism of anticancer properties of PP can help establishing novel and future anti-tumor treatment strategies.

New medication treats drug-resistant prostate cancer in the laboratory

Non-competitive androgen receptor inhibition in vitro and in vivo Pyrvinium inhibits AR-dependent gene expression in the prostate gland in vivo, and induces prostate atrophy. These results highlight new therapeutic strategies to inhibit AR activity.


So far I was in direct contact with two prostate cancer patients who responded to 3BP treatment (one using the oral version and the other using injection). The substance and application approaches are described in this post

4-methylumbelliferone (4-MU)

This element has been often cited as a potential oral chemopreventive, and therapeutic agent that targets PCa development, growth, and metastasis by abrogating HA signaling (Ref.) Sold in Europe under the name Cantabiline (e.g. here). I already discussed 4-MU in this post:

Here are some articles on this subject:

Can a Simple Dietary Supplement Cure Prostate Cancer?

Antitumor activity of hyaluronic acid synthesis inhibitor 4-methylumbelliferone in prostate cancer cells. Therefore, the anticancer effects of 4-MU, an orally bioavailable and relatively nontoxic agent, are primarily mediated by inhibition of HA signaling.

Targeting hyaluronidase for cancer therapy: antitumor activity of sulfated hyaluronic acid in prostate cancer cells.  Taken together, our findings offer mechanistic insights into the tumor-associated HA-HAase system and a preclinical proof-of-concept of the safety and efficacy of sHA to control prostate cancer growth and progression.


Izumi et al. [61] have reported that the treatment with oral TN (300 mg/day) promoted a reduction of prostate-specific antigen (PSA) levels in 4 out of 16 patients with advanced castration-resistant prostate cancer (CRPC). Accordingly, in the subsequent follow-up pilot study, oral treatment with TN (300 mg/day) for a median period of five months documented a continuous PSA inhibition in 3 out of 21 patients with advanced CRPC. Overall survival rates at 12 and 24 months were 74.5% and 61.5%, respectively [167]. As a whole, these results suggest that TN could be used to improve the prognosis of patients with advanced CRPC. However, the two clinical investigations had some limitations: (1) open-label studies with one arm; (2) short follow-up period; (3) small sample size; (4) all patients were Japanese.

Tranilast is a very interesting drug highly relevant against cancers. It is one of a few available to address the specific anti cancer mechanisms that is targeting. However, its accessibility is not the best as it is only available in Japan.


See my post and the references related to prostate cancer.


See my post and the references related to prostate cancer.

Debatable but I think I should mention it: Testosterone

If the cancer is castration-resistant prostate cancer, you may want to discuss the comments at the end of this post and consider this approach This treatment should be essay to access


In case we use hormonal treatment, this may be relevant: The drug ranolazine is a fat oxidation inhibitor that earned FDA approval in 2006 to treat angina. When scientists experimented with fat burning inhibitors and anti-androgens in cancer cell lines, they found that the addition of ranolazine to anti-androgen therapy made tumors more sensitivity to the anti-androgen drug enzalutamide.

Vitamin C and Vitamin K3 and Vitamin E

A 12 Week, Open Label, Phase I/IIa Study Using Apatone® for the Treatment of Prostate Cancer Patients Who Have Failed Standard Therapy Seventeen patients with 2 successive rises in PSA after failure of standard local therapy were treated with (5,000 mg of VC and 50 mg of VK3 each day) for a period of 12 weeks. Prostate Specific Antigen (PSA) levels, PSA velocity (PSAV) and PSA doubling times (PSADT) were calculated before and during treatment at 6 week intervals. Following the initial 12 week trial, 15 of 17 patients opted to continue treatment for an additional period ranging from 6 to 24 months. PSA values were followed for these patients. At the conclusion of the 12 week treatment period, PSAV decreased and PSADT increased in 13 of 17 patients (p ≤ 0.05). There were no dose-limiting adverse effects. Of the 15 patients who continued on Apatone after 12 weeks, only 1 death occurred after 14 months of treatment. Conclusion: Apatone showed promise in delaying biochemical progression in this group of end stage prostate cancer patients.

α-Tocopheryl succinate promotes selective cell death induced by vitamin K3 in combination with ascorbat These finding support the emerging idea that synergistic combinations of some agents can overcome toxicity and other side-effects associated with high doses of single drugs creating the opportunity for therapeutically relevant selectivity.

Alpha-Tocopheryl Succinate Inhibits Autophagic Survival of Prostate Cancer Cells Induced by Vitamin K3 and Ascorbate to Trigger Cell Death α-TOS, a mitochondria-targeting apoptotic agent, switches at sub-apoptotic doses from autophagy-dependent survival of cancer cells to their demise by promoting the induction of apoptosis. Given the grim prognosis for cancer patients, this finding is of potential clinical relevance.


This is a plant extract coming from Traditional Chinese Medicine. It is one of my favorites natural anti cancer extracts and  it has been suggested to act against prostate cancer:

Downregulation of ZFX is associated with inhibition of prostate cancer progression by baicalein Our study provides evidence that baicalein plays important roles in PCa therapy probably by downregulating ZFX expression, which was demonstrated to be involved in PCa progression, and thus may be developed as a novel and efficient candidate agent for PCa therapy

Baicalein inhibits prostate cancer cell growth and metastasis via the caveolin-1/AKT/mTOR pathway In conclusion, these findings suggested that baicalein can induce apoptosis and inhibit metastasis of androgen-independent PCa cells through inhibition of the caveolin-1/AKT/mTOR pathway, which implies that baicalein may be a potential therapeutic agent for the treatment of androgen-independent prostate cancer patients.

Baicalein can be found in whole plant supplements made of Scutellaria baicalensis, or as a pure extract to be ordered on Alibaba website.

Other relevant references:

Molecular pathways and targets in prostate cancer

Human chorionic gonadotropin (hCG) interacts with lovastatin and ionizing radiation to modulate prostate cancer cell viability in vivo.

Suppression of human prostate cancer cell growth by ciprofloxacin is associated with cell cycle arrest and apoptosis

A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy.

Combining the typical hormonal treatment with abiraterone (also used for prostate cancer) seems to lead to improved outcome

A supplement that may very much help specifically for prostate cancer is Boron.

PhD thesis 2016: The role of estrogen receptors in prostate cancer development and their contributions in new treatment opportunities


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37 Comments on "Prostate Cancer"

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D, here are some other good ones.


and next generation

(Apatone) vitamin C and K3


Very interesting as always. I am sure many people will find this helpful!

Clorgyline – antidepressant, may be helpful against bone mets:

Hi Daniel, Thank your for writing a new post about prostate cancer. Yesterday I was at a psychology course about healing and there I spoke with a man who had prostate cancer stage 4 grade 4, who is now cured, even though it is considered at this grade incurable. He based his healing on the faith in God and some energy that God gives you. He goes to the monastery regularly and brings people there, does a lot of good deeds, is helping people and he changed his lifestyle. I wish everyone coming here on the site health and to… Read more »

Hi Daniel,

Very interesting piece!
I have reviewed the role of metformine also recently. The evidence for metformine as anti cancer agent is really strong! But thus far only tested found in diabetics, so there is a caveat.
A doctor is now looking into K3 and cancer for me, as our product is up for review. I keep you updated.


Hi Daniel, I know from you that Metformin is really good in most cancers, but now my mother has such a bad taste in the mouth when taking any drugs (except minerals and vitamins and Melatonin and plants extract) and she says she feels something very chemical in her mouth after taking Metformin. What is your opinion on that? Should she take it, no matter what she feels afterwards? This is the effect of the chemotherapy, and especially Caelyx destroyed her, she could not eat or drink water after Caelyx first session, then she did another one even though Virgil… Read more »
Dear Daniel, Have you heard about a substance called equol? From the wikipedia article: Equol (4′,7-isoflavandiol) is an isoflavandiol metabolized from daidzein, a type of isoflavone found in soybeans and other plant sources, by bacterial flora in the intestines. While endogenous estrogenic hormones such as estradiol are steroids, equol is a nonsteroidal estrogen. However, only about 30% of people in the West have intestinal bacteria that make equol (file:///C:/Users/Ethan/Downloads/metabolites-05-00056-v2.pdf). Equol preferentially binds estrogen receptor beta. By binding to the estrogen receptor, equol may inhibit prostate cancer progression in tumors that have the ERG+ phenotype. Another aspect of its anti-cancer activity… Read more »

Small group of patients have these TRK mutations.
They seem to do very well with this treatment.


Early pre-clinical research, though the drugs are already approved for other indications.
Stopping metastasis would be such a good strategy.

D, the numbers for Loxo look extremely impressive! There is an entirely new generation of very effective cancer treatments that are now emerging. We talked about the strategy of throwing a bunch of darts at the dart board until you hit a bullseye. Loxo101 is one dart. Cancer patients might have a 1% chance of having a TRK fusion, though if they did then LOXO could be such a blessing. If they did not have a TRK fusion, then time for another dart. Loxo is also developing LOXO-292 for RET rearrangements, LOXO-195 second generation TRK, LOXO-305 … LOXO-292 is early… Read more »
Exactly D! This is so critically important from the patient perspective. Knowing that you will probably respond within a 2 month window is very important information. If you have not responded in that window, then you could plan from there. Yet, even several of those who did not respond early, did respond later. It might be very difficult for cancer to work around an anti- fusion treatment Notice that most of the patients had yellow dots after at 2 months. Nearly all of those with a yellow dot than had these prolonged ongoing responses that stretch out to 2 years… Read more »
D, fusion proteins are a very exciting avenue of cancer research! I do not believe people have been fully aware of how important a concept this is. Consider that an onco-fusion protein is highly abnormal; it combines two separate proteins there should be a way to specifically attack it while leaving other cells alone. The anti-fusion drugs have already been successful (Gleevec — BCR-ABL fusion protein in leukemia). The liver patient had a fusion and this might have involved the BSG gene which is of high relevance to 3-BP effectiveness. The TRK patients and the liver patients exhibited ongoing responses… Read more »
Here’s a list of fusions from COSMIC. Really wonder if there might be some more good targets. Would love to know how patients respond to different treatments conditioned on Fusion status. Fusion Samples Mutations Papers BCR-ABL1 8638 5412 233 xxx Gleevec TMPRSS2-ERG 6264 2623 114 xxx 50% of prostate patients EWSR1-FLI1 2132 1332 164 EML4-ALK 11213 701 508 KIAA1549-BRAF 1383 612 79 xxx BRAF CCDC6-RET 6833 593 162 SS18-SSX1 1313 577 135 PML-RARA 545 544 36 PAX3-FOXO1 1163 382 72 NCOA4_ENST00000452682-RET 4431 358 136 ETV6-RUNX1 2277 357 42 FUS-DDIT3 627 351 47 SS18-SSX2 1314 348 136 NPM1-ALK 1344 319… Read more »

D, LOXO-101 is very impressive.

When you look at page numbered 10 in the pdf, you see 6 patients who had tumor growth.
If you notice on the bottom of the page numbered 15, there are 6 patients who never achieved a response and stopped treatment
even before 1.8 months. These patients must have been severely ill. Most trials would not accept them.

Without these patients almost everyone would have achieved at least a response.
When they get this out to real world patients the treatment will do even better.
Think what happens when these patients could be treated at stage 2 or 3!

I am posting this here as it seems the most appropriate place, and the information may help someone else. Standard PET/CT has low sensitivity for prostate cancer, making it difficult to determine the extent and location of early spread. There is a need for more accurate scanning techniques when PET/CT and bone scans are inconclusive. We used the C-11 acetate scan after standard imaging was inconclusive and were then able to determine the exact location of mets. At that time, the Axumin scan had not yet been FDA approved, but now it is, so that one may be the easiest… Read more »