Ivermectin and Fenbendazole Success Stories: Tumors, Melanoma & Chronic Lymphocytic Leukemia

Continuing this Substack’s series on anecdotal repurposed drug case studies is our latest trio of encouraging and incredibly inspirational subscriber comments.

It is painfully obvious by now that the average doctor working on behalf of the Medical Industrial Complex has completely abandoned their Hippocratic Oath; to wit:

A tumor shrinking in half thanks to a combination therapy of Ivermectin and Fenbendaloze should have any oncologist at the very least extraordinarily intrigued, and in a sane world expeditiously organizing an RCT research study so that they may collect their cancer cure Nobel Prize.

But, sadly, oncologists are especially guilty of indifference, more at disdain, for any cancer cures outside of their BigPharma protocols; after all, cancer treatment is the last cash cow standing for their sickcare business model. And thanks to the slow kill bioweapon “vaccines,” the horrifying turbo cancer epidemic is only getting worse.

There is currently a dearth of research into topical Fenbendaloze application, yet this Substack’s subscriber correctly extrapolated on the efficacy of direct skin application:

A research study entitled, Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells corroborates the above comment:

Most metastatic melanoma patients fail to respond to available therapy, underscoring the need for novel approaches to identify new effective treatments. In this study, we screened 2,000 compounds from the Spectrum Library at a concentration of 1 micromol/L using two chemoresistant melanoma cell lines (M-14 and SK-Mel-19) and a spontaneously immortalized, nontumorigenic melanocyte cell line (melan-a). We identified 10 compounds that inhibited the growth of the melanoma cells yet were largely nontoxic to melanocytes. Strikingly, 4 of the 10 compounds (mebendazole, albendazole, fenbendazole, and oxybendazole) are benzimidazoles, a class of structurally related, tubulin-disrupting drugs. Mebendazole was prioritized to further characterize its mechanism of melanoma growth inhibition based on its favorable pharmacokinetic profile. Our data reveal that mebendazole inhibits melanoma growth with an average IC(50) of 0.32 micromol/L and preferentially induces apoptosis in melanoma cells compared with melanocytes. The intrinsic apoptotic response is mediated through phosphorylation of Bcl-2, which occurs rapidly after treatment with mebendazole in melanoma cells but not in melanocytes. Phosphorylation of Bcl-2 in melanoma cells prevents its interaction with proapoptotic Bax, thereby promoting apoptosis. We further show that mebendazole-resistant melanocytes can be sensitized through reduction of Bcl-2 protein levels, showing the essential role of Bcl-2 in the cellular response to mebendazole-mediated tubulin disruption. Our results suggest that this screening approach is useful for identifying agents that show promise in the treatment of even chemoresistant melanoma and identifies mebendazole as a potent, melanoma-specific cytotoxic agent.

Mebendazole-induced microtubule disruption in melan-a, M-14, and SK-Mel-19 cells. Melan-a, M-14, and SK-Mel-19 cells were treated with vehicle alone (A, C, and E) or 0.5 μmol/L mebendazole for 14 h (B, D, and F). After permeabilization and fixation, cells were stained with anti-α-tubulin antibody (red) and 4′,6-diamidino-2-phenylindole (blue). Arrowheads, mitotic figures. Experiment was repeated thrice, with representative images shown.

While the research study concluded oral administration would be the means of treating melanoma…

In conclusion, our data suggest that mebendazole-mediated microtubule disruption results in melanoma-specific phosphorylation of Bcl-2 and subsequent induction of apoptosis. Based on these results as well as its notable safety profile, mebendazole, a well-tolerated, orally available drug, deserves further investigation as a potentially effective treatment for advanced melanoma.

…their in vitro methodology suggests that direct topical application may also induce apoptosis.

Longstanding readers of this Substack know that Mebendazole is identical to Fenbendazole, save for the removal of a single insignificant molecule. The only reason Fenbendazole was altered to produce Mebendazole was to allow BigPharma to price gouge sick patients.

The final success story du jour comes courtesy of a subscriber battling an especially difficult to treat condition:

In a followup email exchange Pepper Jackson wrote the following:

I just got tested 2 days ago! My lymphocyte count is now down to the lowest it has been since 2017. That's 3 years before I was diagnosed with CLL. In the 2017 doctor visit, it was 12, which is more than double what it should have been (around 5), but that doctor just blew it off!

Since my official diagnosis in March 2020, it has fluctuated from 15.9 to 11.7. After testing on the 13th, it is 10.8. Not a big drop, but the best in 7 years. 

I think the combo of IVM and Fenben is working, and I'm sticking with it for as long as it takes to get to a normal count. Thanks!

Clearly, a pattern emerges of insensitive and indifferent oncologists blowing off their patients, rather than thinking outside the box and devising alternative treatment strategies.

We will have an update on Pepper Jackson’s condition when the next round of testing is completed.

They want you dead.

Do NOT comply.