The Anti-Fungal drug Griseofulvin: Like Chemotheraphy but Without its Side Effects

Cellular division:


Mitosis is a part of the cell life cycle in which the division of the nucleus takes place so that finally one cell will become two cells. This is the process in which chromosomes in a cell nucleus are separated into two identical sets of chromosomes, and each set ends up in its own nucleus. The result is two genetically identical daughter nuclei.

Just as our bodies rely on bones for structural support, our cells rely on a cellular skeleton. That is the cytoskeleton which not only helps cells keep their shape but also transports material within cells and coordinates cell division. Thus, during the cell division, the separation of the chromosomes is supported and facilitated by a network of microtubules (component of the cytoskeleton) that transport and align the two chromosomes to opposite sides, at the cell equator.

microtubulesMicrotubules are small tubes, located within the cell’s cytoplasm, with a diameter of about 10-20nm and with their ends designated the (−) and (+) ends. When needed, microtubules can elongate fast, significantly more rapid at the (+) end. The building blocks of microtubule are called α- and β-tubulin. When microtubules elongate at the (+) end, it means that β-subunits are binding while at the (−) end α-subunits are binding.

Indeed, microtubules provide platforms for intracellular transport and (next to chromosomes, centrosomes and a few other proteins – proteins kinesin and dynein – that bind to and serve as “motors” for microtubule dynamics) are the major constituents of mitotic spindles. In this dynamic process, microtubules are nucleated and organized by centrosomes which are small cytoplasmic organelle that act as themicrotubule organizing center.

spindleDuring mitosis, centrosomes function as spindle poles, directing the formation of bipolar spindles, a process essential for accurate chromosomal separation. Centrosomes duplicate precisely once per cell cycle to assure spindle bipolarity, with each daughter cell receiving one centrosome.

In a few words, during mitosis a cell splits its nucleus in two. One part is going one way and the other part goes the opposite direction organised by centrosome and supported by microtubule “arms” with their motors (all under the name of mitotic spindles).

However, in cancer this division leads not only to two separations but to multiple such separations. Such error would immediately trigger cell death in a normal cell. However, cancer cells can overcome this problem by having a mechanism to cluster the centrosomes in to two opposite groups (spindle poles) of multiple centrosomes enabling bipolar cell division.

We have previously seen that this cellular division process can be modulated and inhibited by electro-magnetic fields

Griseofulvin, an inhibitor of fast cellular division

Recent screenings of various drugs have indicated that Griseofulvin, an antifungal FDA approved drug used for fungal nail infections, cheap and available at the pharmacies, induces spindle multipolarity (Ref.). As we discussed above, for cell division bipolarity is required and not multipolarity. Thus, multipolarity induced by Griseofulvin, leads to mitotic arrest, and subsequent cell death in multiple tumor cell lines. This multipolarity induced by Griseofulvin is due to an induction of spindle tension by interaction with and suppression of microtubule dynamics.

As a result, Griseofulvin inhibits microtubule dynamics, which leads to spindle tension, which leads to centrosome declustering in cells with more than two centrosomes, leading to multipolar cell division and ultimately cell death.

Due to its mechanism of action, Griseofulvin behaves in a similar way as chemotheraphies of the Tubulin Interactive agents type, that act by binding to specific sites on tubulin, the building blocks of cellular microtubules. When these agents bind on the protein, the cell can not form microtubules. Tubulin interactive agents include Vincristine, Vinblasune, and Paclitaxel. Griseofulvin shares its binding site in tubulin with paclitaxel and kinetically suppresses microtubule dynamics in a similar manner (Ref.).

Interestingly, it has been suggested that Griseofulvin may be more powerful than Paclitaxel: “Based on our data, RedBr-Nos and Griseofulvin showed more dramatic effects on centrosome declustering and inhibition of neurite formation as compared with PJ-34 and Paclitaxel. In sum, our findings reveal the previously underappreciated aspects of the actions of centrosome-declustering drugs, their potential application as anti-metastatics and the importance of interphase as a chemotherapeutic target.” (Ref.)

Griseofulvin was also suggested to be

  • Wnt inhibitor (Ref.).
  • connexin 43 modulator: “Altogether, these results described a new molecular mechanism connexin 43-dependent targeted by griseofulvin leading to apoptosis of human germ cell tumor cells.” (Ref.)
  • NF-kappaB pathway with cdc-2 activation and phosphorylation of Bcl-2 (Ref.)
  • anti inflammatory (Ref.)

As a side note, Griseofulvin (as well as other microtubule modulators) may also inhibit steroidogenesis (Ref.). This is probably the case in normal adrenal cells since in adrenal cancer cells it seems that Griseofulvin actually leads to an increase of the steroid hormone production such as cortisole, possibly due to adrenal cancer cell apoptosis and release of that, but the mechanism remains still unclear (Ref.).

In view of its ability to stabilize microtubule dynamics and to inhibit microtubule polymerization in human cells, it is remarkable that griseofulvin is well-tolerated when given to humans for the treatment of fungal infections (Ref.) Possibly, the lack of toxicity to normal cells is related to the fact that unlike vincas and taxanes, which inhibit cancer cell proliferation in nanomolar concentration range, Griseofulvin acts in micromolar range. So, the working latitude of Griseofulvin is larger. The lack of significant toxicity of griseofulvin in humans makes this drug relevant as a centrosomal cluster inhibitor.

Due to its mechanism of action, Griseofulvin is relevant for most type of cancers, possibly even more for those fast developing, alone or in combination with other therapies.

Note that a few other drugs that I intend to discuss in other posts, an anti tusive (Noscapine) and an anti worm (Mebendazole) drugs, have similar mode of action as Griseofulvin and consequently are very relevant as potential anti cancer drugs.

Finally, I would like to mention that while Griseofulvin potential as a microtubule dynamics inhibitor is know for long time, one of the first paper highlighting its potential in cancer was published by the German Cancer Research Center from Heidelberg, in 2007 (Ref.). (This to me is a stamp of high quality work. Also note that this is the same center that for the first time applied and demonstrated for the first time the potential of anti cancer effects of Salinomycin in humans.) Following this publication, a website was build to try create awareness about the potential of Griseofulvin in cancer and possibly collect data from patients using it. Here is the link to the website: I suspect this was build by a scientist involved in the German research, who intended to share with the world these relevant findings. However, it seems this website never really reached those potentially interested but hopefully that will change in the future.

In conclusion, here we have a drug that acts as some of the chemotheraphies in the market, but in contrast to those Griseofulvin has a good safety profile and is available to all at very low cost.

In general, all human malignancies are potential targets for centrosomal cluster inhibitors since almost all malignant neoplasias examined to date harbour centrosome aberrations.

Griseofulvin as an anti cancer treatment has been patented already in 1997, by The Procter & Gamble Company (Ref.). After the German Cancer Research Center from Heidelberg confirmed its anti cancer potential and understood the mechanism behind, another patent has been filed by the same organization, focused on improving anti cancer activity and bio-availability (Ref.).

Administartion and dose:

Griseofulvin comes as a tablet, capsule, and liquid to take by mouth.

About two years ago I discussed with doctors at German hospitals administrating this drug to cancer patients with good results. They were administrating to patients at a dose of 1.5g/day (500mg 3x/day). Some patients were taking it daily for several years.

The absorption of griseofulvin is increased by fat in the food. (Ref.)

Safety and Toxicity:

This dose is higher than the 500mg to 1000mg that is recommended. Therefore, the doctors were following the liver function of patients taking the drug. However, no specific issue has been reported.

It may slightly increase heart rate and decrease blood pressure (Ref.).

Although low toxicity (which can not be compared in anyway with that of chemotheraphy) as with most anti fungals, potential side effects do exist. Here is a complete list of potential side effects:


ebay: for example reference

local or online pharmacies: for example


Use of griseofulvin for inhibiting the growth of cancers

A pharmaceutical composition for the treatment of cancers or tumors in mammals is disclosed which comprises griseofulvin. A chemotherapeutic agent can be used in conjunction with griseofulvin as can potentiators. Griseofulvin can also be used to treat viral infections, either alone, in conjunction with other viral agents or with a potentiator.

Identification of Griseofulvin as an Inhibitor of Centrosomal Clustering in a Phenotype-Based Screen

Together with a recent report indicating that griseofulvin, either alone or in combination with nocodazole, inhibits tumor formation in nude mice (47), and in view of its lack of significant toxicity in humans, the data presented here supports the notion that griseofulvin might be useful for the treatment of cancer

Griseofulvin inhibits the growth of adrenocortical cancer cells in vitro

Supernumerary centrosomes and aneuploidy are associated with a malignant phenotype of tumor cells. Centrosomal clustering is a mechanism used by cancer cells with supernumerary centrosomes to solve the threatening problem of multipolar spindles. Griseofulvin is an antifungal substance that interferes with the microtubule apparatus and inhibits centrosomal clustering. It has also been demonstrated that griseofulvin inhibits the growth of tumor cells in vitro and in vivo. However, it is not yet known whether treatment with griseofulvin inhibits growth of adrenocortical tumor cells. We studied the viability and antiproliferative effects of griseofulvin on cultured NCI-H295R adrenocortical carcinoma cells using Wst-1-, BrdUrd-, and [³H]-thymidine assays. For the detection of apoptosis we used a caspase 3/7 cleavage assay and light microscopy techniques. We observed that incubation with griseofulvin for 24-48 h leads to a decrease in the viability and proliferation of NCI-H295R cells in a dose-dependent manner. Significant effects could be observed after incubation with griseofulvin as measured by Wst-1-, BrdUrd-, and [³H]dT- uptake assays. Apoptosis of NCI-H295R cells was increased in a dose-dependent manner up to 4.5-fold after incubation with griseofulvin 40 μM for 24 h as shown by caspase 3/7 cleavage assay and light microscopy. With regard to new treatment strategies for adrenocortical cancer, griseofulvin, and possibly other agents, which interfere with the microtubule apparatus and inhibit centrosomal clustering, may turn out to be interesting targets for further research.

Let’s huddle to prevent a muddle: centrosome declustering as an attractive anticancer strategy:

Nearly a century ago, cell biologists postulated that the chromosomal aberrations blighting cancer cells might be caused by a mysterious organelle-the centrosome-that had only just been discovered. For years, however, this enigmatic structure was neglected in oncologic investigations and has only recently reemerged as a key suspect in tumorigenesis. A majority of cancer cells, unlike healthy cells, possess an amplified centrosome complement, which they manage to coalesce neatly at two spindle poles during mitosis. This clustering mechanism permits the cell to form a pseudo-bipolar mitotic spindle for segregation of sister chromatids. On rare occasions this mechanism fails, resulting in declustered centrosomes and the assembly of a multipolar spindle. Spindle multipolarity consigns the cell to an almost certain fate of mitotic arrest or death. The catastrophic nature of multipolarity has attracted efforts to develop drugs that can induce declustering in cancer cells. Such chemotherapeutics would theoretically spare healthy cells, whose normal centrosome complement should preclude multipolar spindle formation. In search of the ‘Holy Grail’ of nontoxic, cancer cell-selective, and superiorly efficacious chemotherapy, research is underway to elucidate the underpinnings of centrosome clustering mechanisms. Here, we detail the progress made towards that end, highlighting seminal work and suggesting directions for future research, aimed at demystifying this riddling cellular tactic and exploiting it for chemotherapeutic purposes. We also propose a model to highlight the integral role of microtubule dynamicity and the delicate balance of forces on which cancer cells rely for effective centrosome clustering. Finally, we provide insights regarding how perturbation of this balance may pave an inroad for inducing lethal centrosome dispersal and death selectively in cancer cells.

Heading off with the herd: how cancer cells might maneuver supernumerary centrosomes for directional migration.

The complicity of centrosomes in carcinogenesis is unmistakable. Mounting evidence clearly implicates a robust correlation between centrosome amplification (CA) and malignant transformation in diverse tissue types. Furthermore, CA has been suggested as a marker of cancer aggressiveness, in particular the invasive phenotype, in breast and prostate cancers. One means by which CA promotes malignancy is through induction of transient spindle multipolarity during mitosis, which predisposes the cell to karyotypic changes arising from low-grade chromosome mis-segregation. It is well recognized that during cell migration in interphase, centrosome-mediated nucleation of a radial microtubule array is crucial for establishing a polarized Golgi apparatus, without which directionality is precluded. The question of how cancer cells maneuver their supernumerary centrosomes to achieve directionality during cell migration is virtually uncharted territory. Given that CA is a hallmark of cancers and has been correlated with cancer aggressiveness, malignant cells are presumably competent in managing their centrosome surfeit during directional migration, although the cellular logistics of this process remain unexplored. Another key angle worth pondering is whether an overabundance of centrosomes confers some advantage on cancer cells in terms of their migratory and invasive capabilities. Recent studies have uncovered a remarkable strategy that cancer cells employ to deal with the problem of excess centrosomes and ensure bipolar mitoses, viz., centrosome clustering. This review aims to change the narrative by exploring how an increased centrosome complement may, via aneuploidy-independent modulation of the microtubule cytoskeleton, enhance directional migration and invasion of malignant cells. We postulate that CA imbues cancer cells with cytoskeletal advantages that enhance cell polarization, Golgi-dependent vesicular trafficking, stromal invasion, and other aspects of metastatic progression. We also propose that centrosome declustering may represent a novel, cancer cell-specific antimetastatic strategy, as cancer cells may rely on centrosome clustering during migration as they do in mitosis. Elucidation of these details offers an exciting avenue for future research, as does investigating how CA may promote metastasis through enhanced directional migration.

Drugs That Target Dynamic Microtubules: A New Molecular Perspective

Microtubules have long been considered an ideal target for anticancer drugs because of the essential role they play in mitosis, forming the dynamic spindle apparatus. As such, there is a wide variety of compounds currently in clinical use and in development that act as antimitotic agents by altering microtubule dynamics. Although these diverse molecules are known to affect microtubule dynamics upon binding to one of the three established drug domains (taxane, vinca alkaloid, or colchicine site), the exact mechanism by which each drug works is still an area of intense speculation and research. In this study, we review the effects of microtubule-binding chemotherapeutic agents from a new perspective, considering how their mode of binding induces conformational changes and alters biological function relative to the molecular vectors of microtubule assembly or disassembly. These “biological vectors” can thus be used as a spatiotemporal context to describe molecular mechanisms by which microtubule-targeting drugs work.

Griseofulvin stabilizes microtubule dynamics, activates p53 and inhibits the proliferation of MCF-7 cells synergistically with vinblastine

Background: Griseofulvin, an antifungal drug, has recently been shown to inhibit proliferation of various types of cancer cells and to inhibit tumor growth in athymic mice. Due to its low toxicity, griseofulvin has drawn considerable attention for its potential use in cancer chemotherapy. This work aims to understand how griseofulvin suppresses microtubule dynamics in living cells and sought to elucidate the antimitotic and antiproliferative action of the drug.

Methods: The effects of griseofulvin on the dynamics of individual microtubules in live MCF-7 cells were measured by confocal microscopy. Immunofluorescence microscopy, western blotting and flow cytometry were used to analyze the effects of griseofulvin on spindle microtubule organization, cell cycle progression and apoptosis. Further, interactions of purified tubulin with griseofulvin were studied in vitro by spectrophotometry and spectrofluorimetry. Docking analysis was performed using autodock4 and LigandFit module of Discovery Studio 2.1.

Results: Griseofulvin strongly suppressed the dynamic instability of individual microtubules in live MCF-7 cells by reducing the rate and extent of the growing and shortening phases. At or near half-maximal proliferation inhibitory concentration, griseofulvin dampened the dynamicity of microtubules in MCF-7 cells without significantly disrupting the microtubule network. Griseofulvin-induced mitotic arrest was associated with several mitotic abnormalities like misaligned chromosomes, multipolar spindles, misegregated chromosomes resulting in cells containing fragmented nuclei. These fragmented nuclei were found to contain increased concentration of p53. Using both computational and experimental approaches, we provided evidence suggesting that griseofulvin binds to tubulin in two different sites; one site overlaps with the paclitaxel binding site while the second site is located at the αβ intra-dimer interface. In combination studies, griseofulvin and vinblastine were found to exert synergistic effects against MCF-7 cell proliferation.

Conclusions: The study provided evidence suggesting that griseofulvin shares its binding site in tubulin with paclitaxel and kinetically suppresses microtubule dynamics in a similar manner. The results revealed the antimitotic mechanism of action of griseofulvin and provided evidence suggesting that griseofulvin alone and/or in combination with vinblastine may have promising role in breast cancer chemotherapy.

Quantitative multi-parametric evaluation of centrosome declustering drugs: centrosome amplification, mitotic phenotype, cell cycle and death

Centrosome-declustering drugs mediate a two-pronged attack on interphase and mitosis in supercentrosomal cancer cells

Classical anti-mitotic drugs have failed to translate their preclinical efficacy into clinical response in human trials. Their clinical failure has challenged the notion that tumor cells divide frequently at rates comparable to those of cancer cells in vitro and in xenograft models. Given the preponderance of interphase cells in clinical tumors, we asked whether targeting amplified centrosomes, which cancer cells carefully preserve in a tightly clustered conformation throughout interphase, presents a superior chemotherapeutic strategy that sabotages interphase-specific cellular activities, such as migration. Herein we have utilized supercentrosomal N1E-115 murine neuroblastoma cells as a test-bed to study interphase centrosome declustering induced by putative declustering agents, such as Reduced-9-bromonoscapine (RedBr-Nos), Griseofulvin and PJ-34. We found tight ‘supercentrosomal’ clusters in the interphase and mitosis of ~80% of patients’ tumor cells with excess centrosomes. RedBr-Nos was the strongest declustering agent with a declustering index of 0.36 and completely dispersed interphase centrosome clusters in N1E-115 cells. Interphase centrosome declustering caused inhibition of neurite formation, impairment of cell polarization and Golgi organization, disrupted cellular protrusions and focal adhesion contacts—factors that are crucial prerequisites for directional migration. Thus our data illustrate an interphase-specific potential anti-migratory role of centrosome-declustering agents in addition to their previously acknowledged ability to induce spindle multipolarity and mitotic catastrophe. Centrosome-declustering agents counter centrosome clustering to inhibit directional cell migration in interphase cells and set up multipolar mitotic catastrophe, suggesting that disbanding the nuclear–centrosome–Golgi axis is a potential anti-metastasis strategy.

Effects of griseofulvin on apoptosis through caspase-3- and caspase-9-dependent pathways in K562 leukemia cells: An in vitro study

These findings suggest that griseofulvin inhibited growth of K562 cells and induced cell apoptosis through cell-cycle arrest and mitochondrial membrane potential decrease as well as caspase-3 and -9 activation. Further testing is needed to evaluate the potential of griseofulvin as a candidate in the chemotherapy of hematologic malignancies.

Griseofulvin potentiates antitumorigenesis effects of nocodazole through induction of apoptosis and G2/M cell cycle arrest in human colorectal cancer cells.

In this study, we demonstrate that apoptosis and G2/M cell cycle arrest were easily induced by treatment with the oral-antifungal agent, griseofulvin (GF). The mechanisms of GF-induced G2/M arrest were characterized as (a) induction of abnormal mitotic spindle formation, (b) elevation of cyclin B1/cdc2 kinase activity and (c) down-regulation of myt-1 protein expression. On the other hand, caspase 3 activation, Bcl-2 hyperphosphorylation and inhibition of the normal function of Bcl-2 associated with Bax were demonstrated to be the mechanisms of GF-induced apoptosis. DNA fragmentation and flow cytometry analyses demonstrated that combined treatment of GF with the cancer chemotherapeutic agent, nocodazole (ND), strongly potentiates the apoptotic effect and arrest of the G2/M cell cycle in 5 types of human cancer cells, but not in normal human keratinocytes (#76 KhGH). The combined treatment of GF and ND triggered the polymerization of purified tubulin in HT 29 but not in #76 KhGH cells. To further confirm these observations, the therapeutic efficacy was further examined in vivo by treating athymic mice bearing COLO 205 tumor xenografts, with GF (50 mg/kg), ND (5 mg/kg) or GF + ND. Combined treatment of GF and ND significantly enhanced the effect of ND, and led to cessation of tumor growth. These results suggest that chemotherapeutic agents (such as ND) administered in the presence of GF might provide a novel therapy for colorectal cancer.

Kinetic suppression of microtubule dynamic instability by griseofulvin: implications for its possible use in the treatment of cancer.

The antifungal drug griseofulvin inhibits mitosis strongly in fungal cells and weakly in mammalian cells by affecting mitotic spindle microtubule (MT) function. Griseofulvin also blocks cell-cycle progression at G(2)/M and induces apoptosis in human tumor cell lines. Despite extensive study, the mechanism by which the drug inhibits mitosis in human cells remains unclear. Here, we analyzed the ability of griseofulvin to inhibit cell proliferation and mitosis and to affect MT polymerization and organization in HeLa cells together with its ability to affect MT polymerization and dynamic instability in vitro. Griseofulvin inhibited cell-cycle progression at prometaphase/anaphase of mitosis in parallel with its ability to inhibit cell proliferation. At its mitotic IC(50) of 20 muM, spindles in blocked cells displayed nearly normal quantities of MTs and MT organization similar to spindles blocked by more powerful MT-targeted drugs. Similar to previously published data, we found that very high concentrations of griseofulvin (>100 microM) were required to inhibit MT polymerization in vitro. However, much lower drug concentrations (1-20 microM) strongly suppressed the dynamic instability behavior of the MTs. We suggest that the primary mechanism by which griseofulvin inhibits mitosis in human cells is by suppressing spindle MT dynamics in a manner qualitatively similar to that of much more powerful antimitotic drugs, including the vinca alkaloids and the taxanes. In view of griseofulvin’s lack of significant toxicity in humans, we further suggest that it could be useful as an adjuvant in combination with more powerful drugs for the treatment of cancer.

Centrosome-declustering drugs mediate a two-pronged attack on interphase and mitosis in supercentrosomal cancer cells

Comparison of the aneugenic properties of nocodazole, paclitaxel and griseofulvin in vitro. Centrosome defects and alterations in protein expression profiles.

In vivo efficacy of griseofulvin against multiple myeloma

Microtubule assembly dynamics: an attractive target for anticancer drugs.

Microtubules, composed of alphabeta tubulin dimers, are dynamic polymers of eukaryotic cells. They play important roles in various cellular functions including mitosis. Microtubules exhibit differential dynamic behaviors during different phases of the cell cycle. Inhibition of the microtubule assembly dynamics causes cell cycle arrest leading to apoptosis; thus, qualifying them as important drug targets for treating several diseases including cancer, neuronal, fungal, and parasitic diseases. Although several microtubule-targeted drugs are successfully being used in cancer chemotherapy, the development of resistance against these drugs and their inherent toxicities warrant the development of new agents with improved efficacy. Several antimicrotubule agents are currently being evaluated for their possible uses in cancer chemotherapy. Benomyl, griseofulvin, and sulfonamides have been used as antifungal and antibacterial drugs. Recent reports have shown that these drugs have potent antitumor potential. These agents are shown to inhibit proliferation of different types of tumor cells and induce apoptosis by targeting microtubule assembly dynamics. However, unlike vincas and taxanes, which inhibit cancer cell proliferation in nanomolar concentration range, these agents act in micromolar range and are considered to have limited toxicities. Here, we suggest that these drugs may have a significant use in cancer chemotherapy when used in combination with other anticancer drugs.

Synthesis and activities towards resistant cancer cells of sulfone and sulfoxide griseofulvin derivatives.

Griseofulvin, an antifungal drug, has been shown in recent years to have anti-proliferative activities. We report here the synthesis of new analogs ofgriseofulvin, substituted in 2′ by a sulfonyl group or in 3′ by a sulfinyl or sulfonyl group. These compounds exhibit good anti-proliferative activities against SCC114 cells, an oral squamous carcinoma cell line showing pronounced centrosome amplification, and unexpected cytotoxic activities on HCC1937 cells, a triple negative breast cancer cell line resistant to microtubule inhibitors.


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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Thank you so much Daniel

about my mother , the tumor marker was 712 , the doctor changed from taxotere to another combination of chemo (Vinorelbine + 5-FU)

and the DCA was arrived , after 3 weeks the first cycle (first week taking chemo , other 2 weeks DCA) the tumor marker fall to 670 (not too much)

but it was only the beginning , after taking another cycle (chemo + DCA) combination the tumor marker fall to 460 !
this is a very good result 🙂

I’m still trying to get Escozul , but due to our economic problems its still hard to buy anything from the internet .

but sure I cant ignore your great article about artmisinin , propranolol and Griseofulvin

so I decided to bring them all 😀

thanks a lot


I hope to cancel the chemo as soon as i can, especially because my mother is taking chemo from about 9 months

but we can’t risk stopping chemo now, if its effective we will like to continue until the markers fall under 100

after that we will bring all the other choices from Griseofulvin to Salinomycin :-p

about DCA , in the past my mother was taking (DCA + Taxotere) 1 cycle = 3 weeks
the first week Taxotere , the other 2 weeks DCA , the dose is 20mg/kg + 600mg vitamin B1 Daily

the last time , doctor changed to (Vinorelbine + 5-FU) , 1 cycle = 4 weeks (28 days)
the first 10 days (Vinorelbine + 5-FU) , the other 18 days DCA , 25mg/kg + 600mg vitamin B1 Daily

I learned about DCA protocols from Dr. Akbar Khan , i also learned about 3-BP from him , and that what brings me to your discussion at cancer compass , and finally i find my self here 😀

thank you so much


about 6 months ago I tried this combination , chemo + DCA at the same time at the same day , I didn’t notice any difference , but I tried it just for 1 cycle only

Dr, Akbar Khan said that taking DCA with chemo at the same time may boost the effect or interfere as well

so his strategy is not to take chemo and DCA at the same time (the same day) , doing some tests will show if its good to take chemo + DCA together or not , here you can watch about his research in 2014

I don’t know if you see this video before , and I’m not sure if he is right about every thing he said

about Griseofulvin , it’s easy to get it just like Propanolol , but I need to check the liver enzymes to make sure that things are going good 🙂

Salinomycin , Escozul and the others are not easy to get , it will take some time , I hope it will be soon …

Momma boy
Momma boy

Can you take it if you are not undergoing chemo?


i wanted to ask you what you think about this drug and then i found this article…:)


anyone knowing a reliable source for griseofluvin please let me know. the pagge above is not accepting normal payments, only bitcoin, i dont want to mess with it. on ebay etc there is no result. in my country a doctor needs to prescribe it…


Hello Daniel.
First of all, thank you for this site full of good advices. It is so helpful for my father who has stage 4 stomach cancer!

Today i would like to ask you if you have any idea which one is more efficient agains cancer : Mebendazol or Grisefuline? I saw that both have a similar effect, so do we have to choose to use just one of them?!
My father started taking Mebendazol this summer but it is difficult to get it in France. Mebendazol is not sold here. However, if Mebendazol is better or if it is dangerous to stop it and start Grisefuline, we will try to continue with it.
Thank you very much.