Bicalutamide: Difference between revisions
From Proteopedia
Jump to navigationJump to search
No edit summary |
No edit summary |
||
| Line 10: | Line 10: | ||
Nonetheless, the AR has some structural singularities that may not let this change of conformation. One of the most important changes is the additional C-terminal region in H12 anchored to the receptor by the formation of a ß-sheet, limiting its movement <ref name="ARA prostate" /><ref name="MoA" />. Due to this structural difference, ''in silico'' approaches have suggested that the antiandrogen effect of bicalutamide may be produced by the instability of the homodimer <ref name="MoA" />. That may lend to the dissociation of the homodimer preventing the transcriptional activity of the AR and explaining the mechanism of action of this drug <ref name="MoA" />. In addition,'' in silico'' analysis have shown that the W741L mutation leads to a more stable bicalutamide-AR homodimer, which may provide some insight into the withdrawal syndrome observed in bicalutamide treatment <ref name="MoA" />. | Nonetheless, the AR has some structural singularities that may not let this change of conformation. One of the most important changes is the additional C-terminal region in H12 anchored to the receptor by the formation of a ß-sheet, limiting its movement <ref name="ARA prostate" /><ref name="MoA" />. Due to this structural difference, ''in silico'' approaches have suggested that the antiandrogen effect of bicalutamide may be produced by the instability of the homodimer <ref name="MoA" />. That may lend to the dissociation of the homodimer preventing the transcriptional activity of the AR and explaining the mechanism of action of this drug <ref name="MoA" />. In addition,'' in silico'' analysis have shown that the W741L mutation leads to a more stable bicalutamide-AR homodimer, which may provide some insight into the withdrawal syndrome observed in bicalutamide treatment <ref name="MoA" />. | ||
For future research, it will be useful to understand the precise mechanism of action of antiandrogens currently used in the clinic, with the objective of developing new drugs which can escape from the antagonist-agonist switch seen in bicalutamide or flutamide. One example of this is apalutamide, a non-steroidal second generation antiandrogen <ref name="ARA prostate" /><ref name="Role of AR" />, approved for use in non metastatic castration resistant prostate cancer patients by the FDA in 2018 <ref name="Role of AR" />. See also the [https://clinicaltrials.gov/ct2/show/NCT01946204 SPARTAN study]<ref>PMID: 29420164</ref>. This new drug has promising uses but it is still associated with side effects like an increased level of falls in patients with the treatment vs placebo <ref>PMID: 36209239</ref>. | For future research, it will be useful to understand the precise mechanism of action of antiandrogens currently used in the clinic, with the objective of developing new drugs which can escape from the antagonist-agonist switch seen in bicalutamide or flutamide. One example of this is apalutamide, a non-steroidal second generation antiandrogen <ref name="ARA prostate" /><ref name="Role of AR">PMID: 30209899</ref>, approved for use in non metastatic castration resistant prostate cancer patients by the FDA in 2018 <ref name="Role of AR" />. See also the [https://clinicaltrials.gov/ct2/show/NCT01946204 SPARTAN study]<ref>PMID: 29420164</ref>. This new drug has promising uses but it is still associated with side effects like an increased level of falls in patients with the treatment vs placebo <ref>PMID: 36209239</ref>. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 13:51, 7 January 2024
| ||||||||||||