A synthetic compound has a impressive ER-alpha binding affinity, comparable to the clinical standard but feeble anti-proliferation activity on breast cancer cells line. What are the possible reason and speculations which can be deduced from such observations.
Keeping aside experimental errors as all experiments were in triplicate and independent.
There could be many possibilities to this observation:
1) Probably in cell based assay, compound have some physio-chemical limitation which diminishes its full binding affinity or makes it less active, or
2) Could be possible that ER receptor have another type of surface topology in its orthosteric binding site in these cancer cell lines, which could be related to the possible mutations or resulted from any aberrant hetro-dimerization or homo-dimerization of these receptors,
or
3) May be, cell lines are more dependent on some other signalling which is alternative to ER-signalling for their survival,
or
4) Possibly, compound have multiple targets which together neutralize the effect,
or
5) Could be possible that the compound binds to some other protein more potent than ER receptor,
or
6) Could be resulted of one or many above mentioned points together.
Also, I believe there could be possibly many more conclusions can be drawn with this kind of observation, unless few experiments needs to perform to subside the possibilities.
Good Luck
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