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Ivermectin for t(4;14) Myeloma
What is the potential of ivermectin for t(4;14) myeloma? According to the researched linked below ivermectin has anti-mm action and it was “observed that ivermectin induced apoptosis in t(4;14) MM cells…”
So that means that ivermectin is a viable therapy for MM patients, right? Well, not exactly. I am a cautious as anyone about the possible toxicity of FDA approved MM therapies. But even I will admit that the process that the FDA goes through to approve a MM therapy includes specific information about dosing.
Information that is missing from both articles below. Which means that yes, ivermectin can kill MM and it can enhance the efficacy of velcade aka bortezomib. But in a “time and dose dependent manner.” Which I think means, the more the better.
3 Things To Know Before Using Ivermectin
I am a long-term MM survivor. No one wants to see MM therapies developed more than I do. But I’ve learned that managing MM is about more than killing MM cells. In my experience possible side effects, toxicity, etc. is as important as the ability of a medication to kill MM.
Do you have MM? Email me at David.PeopleBeatingCancer@gmail.com with questions about both conventional and non-conventional MM therapies.
Thank you,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Gene signatures to therapeutics: Assessing the potential of ivermectin against t(4;14) multiple myeloma
“Multiple myeloma (MM) is a terminal differentiated B-cell tumor disease characterized by clonal proliferation of malignant plasma cells and excessive levels of monoclonal immunoglobulins in the bone marrow. The translocation, (t)(4;14), results in high-risk MM with limited treatment alternatives…
Ivermectin inhibits the proliferation of t(4;14) MM cells
We evaluated the impact of ivermectin on t(4;14) MM cell proliferation by subjecting cells to varying concentrations (0, 4, 6, 8, 10, and 20 µmol/L) of ivermectin and time intervals (24 and 48 h) of exposure. Cell viability, determined using CCK8, demonstrated a significant, concentration- and time-dependent decrease in cancer cell viability (Figure 3A and B)…
Ivermectin induces apoptosis in t(4;14) MM cells
Drug-induced apoptosis is the primary mechanism underlying cancer cell death[18]. To assess this, we analyzed the expression of the pro- and anti-apoptotic proteins BAX and BCL2, respectively, after treatment and further inspected the BAX/BCL2 ratio. We observed that ivermectin induced apoptosis in t(4;14) MM cells, as evidenced by the upregulation of pro-apoptotic protein BAX and a decrease in anti-apoptotic protein BCL2 levels (Figure 3C)…
CONCLUSION
In conclusion, we utilized bioinformatics tools, molecular docking, and experimental validation to identify key genes and potential treatments for t(4;14) MM. Notably, we confirmed that ivermectin induced apoptosis in t(4;14) MM cells via the NF-κB signaling pathway. However, these insights require additional exploration and robust validation in further studies.”
Combinations of ivermectin with proteasome inhibitors induce synergistic lethality in multiple myeloma
Highlights
- Ivermectin, a mature macrolide drug, exerts antimyeloma effects.
- Ivermectin targeted multiple myeloma cells via inhibiting nuclear proteasome activity and inducing DNA damage.
- Ivermectin significantly synergized with proteasome inhibitors in vitro and in vivo.
- The combination of ivermectin with bortezomib was well tolerated by experimental animals.
Ivermectin combined with proteasome inhibitors induces more potent anti-multiple myeloma activity
Since bortezomib (BTZ) is widely used as a first-line therapeutic agent in MM treatment, we next evaluated whether the combination of IVM and BTZ induced synergistic cytotoxicity toward MM cells…
The apoptosis assay showed that low doses of the dual-drug treatment induced MM cell death in all tested MM cell lines (Fig. 4B–C)…
Ivermectin cotreated with bortezomib has unremarkable organ toxicity in mice
To evaluate the drugs’ toxicity in vivo, we treated Balb/c mice with IVM, alone or in combination with BTZ, at different dosages. The mice treated with IVM (2 mg/kg) alone or in combination with BTZ (0.5 mg/kg) had mild myelosuppression 3 days after treatment, with a reduction in reticulocytes, platelets, leukocytes, and neutrophils (Fig. 5A). However, the counts of blood cells returned to normal from days 7–14 (Fig. 5A, Fig. S3A)…
In summary, our findings supported the clinical development of IVM in MM treatment. We also provided a framework of IVM usage in which IVM-BTZ dual-drug treatment might be promising in MM treatment.”
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