ACP-105: Benefits, Mechanism of Action and Dosage
Feb 6,2025
ACP-105, biochemically known as 2-Chloro-4-[(1R,5R)-3-hydroxy-3-methyl-8-azabicyclo[3.2.1]octan-8-yl]-3-methyl benzonitrile, is a potent Selective Androgen Receptor Modulators, commonly known as SARMs.
Mechanism of action
ACP-105, like many other SARMs, works by selectively binding to androgen receptors. With this preferable binding, ACP-105 doesn’t cause unnecessary effects on other vital organs of our body.
Besides this, ACP-105 helps reduce the levels of high-density lipoproteins alongside increasing lean muscle mass.
Additionally, due to a lack of aromaticity, the compound does not induce an increase in estrogen levels, thereby decreasing water retention.
ACP-105 indeed has increased potency and stronger anabolic effects; however, it still does not surpass the potential benefits of testosterone. Nonetheless, this makes ACP-105 much safer to use.
Benefits
ACP-105 is a non-steroidal androgen receptor (AR) agonist. It increases proliferation in a receptor selection and amplification technology (R-SAT) assay using NIH3T3 cells expressing AR or AR containing a tyrosine-to-alanine substitution at position 877 (ART887A; EC50s = 1 and 0.4 nM, respectively).
Dosage
ACP-105 (1 mg/kg per day) inhibits radiation-induced decreases in contextual fear conditioning freezing time, indicating a reversal of memory deficits, in female mice. It reduces the frequency of time spent in the external and intermediate zone in an open field test, indicating anxiolytic-like activity, in combination with the non-steroidal estrogen receptor β (ERβ) agonist AC-186 in a gonadectomized 3xTg mouse model of Alzheimer's disease when administered at a dose of 10 mg/kg per day for four months. ACP-105 (10 mg/kg per day for seven months), in combination with AC-186, decreases amyloid-β (1-40) (Aβ40) and Aβ42 levels in the brains, as well as increases the levels of ARs and the amyloid-β degrading enzymes neprilysin and insulin-degrading enzyme in the hippocampus, of gonadectomized 3xTg mice.
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