Brain Cancer

Relevant drugs/supplements/protocols for brain cancer:

Most of the above are accessible to anyone in terms of price and availability.

Based on my readings so far, it becomes apparent that intracellular Cl modulation is a way to target GMB. Drugs or supplements that can modulate Cl channels are:

Other relevant references:


This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

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13 thoughts on “Brain Cancer

  1. It is a comprehensive list, but I would add Macitentan to it, paper:
    Macitentan, a Dual Endothelin Receptor Antagonist, in Combination with Temozolomide Leads to Glioblastoma Regression and Long-term Survival in Mice.
    Macitentan inhibits pathways linked to proliferation, angiogenesis, invasion, metastasis and chemoresistance.

  2. Dear Daniel,
    How are you?

    With relation to the possible use of macitentan for GBM that you mentioned in this thread ( from Oct 2015), which I also saw @ovidiu mentioned in the drug cocktail (COC protocol) thread,

    I AM REALLY THRILLED with these amazing results! I don’t think I saw another case (even in lab with mice) of a complete GBM remission and we sure all wish it could be reproduced!

    Then, I managed to find 2 clinical trials with macitentan + TMZ for cancer (GBM):
    a) / Jan 2012 for 1 year – phase 1/1b trial: macitentan+TMZ for recurrent GBM [75 patients] – Results: “Terminated (Results did not clearly support continuing development in recurrent GBM)”
    b) / Jan 2015 for 3 years- phase 1 trial: macitentan+TMZ for newly diagnosed GBM or gliosarcoma [ 30 patients] – Results: “Terminated (Sponsor decision due to low recruitment)”

    I must say that considering the amazing results in vivo with mice from 2015, I became a bit confused/ suspicious about these technical/ unclear terminations of the 2 clinical trials…

    1. In case you have any idea or additional info about the results of the 1st trial from 2012 (or other trial I might have missed) we will be happy to hear about it.

    2. in the trial with mice, the macitentan dosage was 10mg/ KG/ day.
    So, if we want to reproduce this with a patient, should he take also 10mg/ kg/ day? remark – I saw the documentation of this drug states 10mg/ day as the maximal dosage for treating PAH (pulmonary arterial hypertension) and the 2 above trials set 150mg and up to 375mg macitentan.

    Many thanks!
    Best wishes!

    1. HI Nissim,

      Next to the info from Johan, on this page (in the drug related section) I shared a file that is often used in the labs to make the conversion. Conversion of mice to man requires to apply a 1/12 factor. That would lead to 0.833mg/kg/day for humans. That would be about 60mg/day for a 70kg person. In the clinical trial they probably pushed the dose as high as possible while being safe.

      Kind regards,

  3. Hi Nissim!
    I was studying a good time macitentan for gbm, in fact I was about to acquire it but the results of the clinical trials you mentioned disappointed me.
    I have followed the use in several patients and chose not to use it for my mother. It is possible that within a “cocktail” therapy is more effective but I had to opt for other molecules.
    In this brain tumor blog you will find several discussions about macitentan:
    My best wishes!

  4. Dear Danial and all,

    I hope you are all OK and successful with your treatments and help

    My brother is using Novocure TTF (Tumor Treating Fields) device for the last few months as one of the treatments for GBM.

    A few days ago we got a link to an interesting lab study results from 2017, named “Synergistic Inhibition of Glioma Cell Proliferation by Withaferin A and Tumor Treating Fields” –
    Remark – I understand that Withaferin A is made from “ashwagandha tree”

    In this study they used Withaferin A with TTF and found that this combination significantly inhibited the growth of the glioma cells to a degree beyond that of Withaferin A or TTF treatment alone.
    Remark – They also refered to an earlier study where Withaferin A was shown to inhibit the growth of several glioma lines at an IC50 of 250 nM –

    In the study they tested several concentrations of Withaferin A (0 to 0.3 μM) combined with TTF and found out that concentration of 0.1 μM or above gave the same improvement (at 0 μM there was no improvement).

    Q – My question is regarding the transformation calculation of the Withaferin A concentration used with cell lines in lab (0.1 μM) to human dosage. What should be considered for this?

    Any help will be appreciated!

    Thank you as always!
    Beat regards,

  5. Hi Daniel and everyone!
    How are you doing? I sure hope you are all ok and health situation is improving!

    I happened to find this study about the possible use of relatively old antihistamine, named clemastine (Tavegil) to fight and kill invasive glioblastoma cells.

    Brief summary:
    This study mention the fact that invasive gbm cells are chemoresistant, impossible to remove by surgery, and cause tumour relapses.
    Also, the heart‐specific, fatty‐acid binding protein 3 (MDGI/FABP3), was highly expressed in mesenchymal glioblastomas, and its high expression correlated with poor patient survival.

    Yet, this study identified the vulnerability of invasive glioblastomas for lysosomal leakiness, regulated by MDGI/FABP3, and induced in vitro and in vivo by cationic amphiphilic drugs (CAD).

    LMP (lysosomal membrane permeabilisation) inducement by some drugs (for example by clemastine) cause to MDGI silencing, which in turn dramatically compromised the viability of patient‐derived glioblastoma cells in vitro and impaired neoplastic initiation in vivo, while its overexpression promoted tumour invasiveness.
    MDGI silencing led to progressive depletion of intracellular phospholipids essential to the integrity of lysosomal membranes, which induced caspase‐independent glioma cell death via LMP.

    Thus using clemastine might kill invasive gbm cells.

    As much as I understood, clemastine is an over the counter drug in USA.
    I also found several threads about the possible benefit of using clemastine for the treatment of multiple sclerosis (MS).

    Did anyone heard of its possible use?
    Any remarks on this study are appreciated.

    Many thanks and best wishes!

      1. Hi everyone,

        After also getting additional information from the Prof’ who managed this study,
        we got also a reference of a trial that used clemastine for MS (Multiple Sclerosis). in this study the participants got 5.36 mg clemastine fumarate (as I understood it is eq’ to 4 mg clemastine) x 2 / day, for 90 days with no special side effects, except for drowsiness, which is the major common side effect when using clemastine.

        We managed to find an online pharmacy in the UK that we can buy clemastine (Tavegyl) and when we’ll get it we’ll have to see how to incorporate it into the current protocol, while hoping for minimum or no drowsiness.

        Any further comments/ remarks are appreciated!

        Health and a happy new year to you all!

        Best wishes,

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