General Comments / Chat, page-6158

Is Zantrene secretly an FLT3 Inhibitor?

Started looking at this to see if how FluClo combination might synergy with Zantrene, is it due to FluClo induced FTO resistance. It doesnt not appear to be the case on face value. But perhaps another pathway FLT3 has some answers.

The IC50 for AML mutation FLT3-ITD is 16 meaning this subtype of AML is extremely sensitive to Zantrene. Whilst we know that AML overexpresses FTO this seems to have even greater killing power against FLT3 subtypes.



The following table shows the survival of FLT3 subtype 'black line' against other AML subtypes.


Source: 999900215e618e67ff0dab19db4a9048 (sharelinktechnologies.com)



Source: adv_q2_15_cancer_final_060115-summer.pdf (massgeneral.org)

General observation only is that MEK inhibitors, pathways in the Melanoma preclinical results and overcame resistance in Melanoma completely separate from AML.

The was repeated in the MD Anderson results where Zantrene + Flu provided synergy more than the two drugs independently.

Source; MD Anderson Cancer Center Researchers Publish AML Preclinical Study on Zantrene® Drug Combinations – Race Oncology

In summary, if fludarabine kills cancer, Zantrene kills more cancer due to FTO expression / as a single agent but together kills even more cancer. Is the synergy the result of Zantrene overcoming fludarabine resistance caused by FLT3 or induced FTO expression. If so this provides a broader commercial opportunity than FTO.

FTO may be how it achieves this but leaves endless opportunities on the table if via another pathway (directly or indirectly).

In my view it is important to understand the Mechanism of Action of Zantrene to maximise commercial outcomes. This reinforces the importance of the upcoming results from Biomarker / Genomic and Companion diagnostic, which could be significant. Or, simply point back to FTO being the only driver in overcoming resistant / synergy.

Think this AGM is going to be a cracker, pity I can't attend.