
ACP-105 | Pen
ACP-105 is a SARM positioned for controlled research settings where androgen receptor–selective anabolic signaling is being studied in relation to lean mass and hypertrophy endpoints, bone density/turnover markers, and tissue-selective androgenic load (e.g., prostate-associated markers).
Supports
- Androgen receptor (AR) activation with muscle- and bone-biased signaling (model-dependent)
- Lean mass preservation and hypertrophy endpoints during catabolic or immobilization paradigms
- Functional strength and load-resistance readouts in musculoskeletal models
- Bone mineral density and bone turnover marker modulation in osteopenia paradigms
- Endocrine-axis feedback markers (LH/FSH/testosterone panels) under AR modulation protocols
Description
ACP-105 is a non-steroidal selective androgen receptor modulator (SARM) investigated for anabolic-biased signaling in skeletal muscle and bone with comparatively limited androgenic activity in non-target tissues. In experimental pharmacology, compounds in this class are evaluated for their ability to separate anabolic effects (muscle/bone) from androgenic effects (e.g., prostate-associated endpoints) using standardized in vitro assays and androgen-deprived animal models.
Research positioning for ACP-105 often centers on models of sarcopenia-like muscle loss, immobilization or disuse atrophy, and osteopenia paradigms where bone density and strength outcomes can be tracked alongside muscle endpoints. As with other SARMs, mechanistic interpretation depends on receptor activation profiles, tissue distribution, study duration, and the specific endpoint framework used to quantify “anabolic vs androgenic” separation.
ACP-105 is presented for research context only. Outcomes and safety signals are protocol-dependent and should be interpreted within controlled laboratory design with appropriate endocrine and tissue monitoring.
Clinical Status
Publicly available evidence for ACP-105 is primarily preclinical (in vitro receptor assays and animal models) and class-based SARM literature describing tissue selectivity frameworks. Human randomized clinical trial evidence specific to ACP-105 is not established as a primary basis for interpretation.
Evidence type:
Human RCT ☐ | Observational ☐ | Animal ✔ | In vitro ✔ | Regulatory approval ☐
Mechanism of Action
ACP-105 binds to the androgen receptor and is studied for promoting anabolic transcriptional programs in muscle and bone, including pathways linked to protein synthesis and musculoskeletal remodeling. In SARM research, tissue selectivity is evaluated by comparing anabolic readouts (e.g., levator ani or muscle mass proxies, bone strength markers) against androgenic surrogate endpoints (e.g., prostate/seminal vesicle measures) in androgen-deprived models.
As a non-steroidal AR ligand, ACP-105 is positioned to avoid classic steroid conversion pathways (e.g., aromatization to estrogens) in mechanistic interpretation, though downstream endocrine feedback (HPT axis signaling) can still shift depending on exposure duration and model sensitivity. Therefore, endocrine panels and tissue-selectivity endpoints are typically included in robust experimental designs.
Benefits
-
Muscle-directed anabolic endpoints:
Studied for increasing or preserving lean mass and hypertrophy markers in controlled muscle-loss and rehabilitation paradigms. -
Bone density and strength research:
Positioned for osteopenia and bone remodeling models that track BMD and bone turnover markers alongside muscle outcomes. -
Functional strength readouts:
Used in protocols assessing load-resistance, grip/force proxies, and functional performance measures in musculoskeletal research. -
Tissue selectivity profiling:
Evaluated for reduced relative androgenic activity in prostate-associated surrogate endpoints compared with anabolic effects in muscle/bone. -
Endocrine stability benchmarking:
Included in studies that monitor LH/FSH/testosterone and related markers to quantify axis effects across protocol lengths. -
Comparative SARM design space:
Often discussed relative to better-known SARMs (e.g., MK-2866, LGD-4033, S23) to compare potency vs tolerability profiles in matched assays.
Research Data
| Study/model | Reported effect |
| AR binding and transactivation assays (in vitro) | AR ligand activity characterized through receptor binding and transcriptional activation endpoints (potency/selectivity dependent on assay) |
| Androgen-deprived rodent SARM profiling (animal) | Anabolic vs androgenic separation evaluated using muscle proxies (e.g., levator ani) and prostate-associated surrogate endpoints |
| Disuse/immobilization paradigms (animal) | Lean mass preservation and force-related readouts assessed under reduced-activity muscle loss conditions (model-dependent) |
| Osteopenia models (animal) | BMD and bone turnover markers tracked alongside muscle outcomes to map musculoskeletal co-effects |
| Gene expression profiling in muscle/bone tissues | AR-responsive transcriptional signatures measured to compare SARM vs testosterone pathway engagement patterns |
| Endocrine feedback monitoring (animal) | LH/FSH/testosterone marker shifts used to quantify axis response to AR modulation across durations |
| SARM class safety signal literature | HPT-axis suppression risk signals and liver-related monitoring discussed for the class in misuse contexts; compound-specific data vary |
| Analytical verification workflows | LC–MS/MS methods used for identity confirmation and exposure verification in research/monitoring contexts |
Stack Suggestions
In extended experimental designs, ACP-105 is sometimes paired with:
- MK-677 (Ibutamoren) → to co-study GH/IGF-axis markers alongside AR-driven anabolic endpoints
- SS-31 (Elamipretide) → to explore mitochondrial stress markers in parallel with strength and recovery readouts
- BPC-157 → to examine tissue-repair and remodeling endpoints alongside disuse/rehabilitation paradigms
Stacks discussed are for experimental design only, not safety/efficacy guidance.
Possible Side Effects
Within the existing observations, ACP-105 shows a good tolerability profile. However, under certain conditions the following reactions can be reported:
• Temporary suppression of endogenous androgen production;
• Variable individual sensitivity to receptor stimulation;
• Lack of sufficient data on safety with long-term use.
Compliance with the optimal dosage and control over the duration of the application play a key role in limiting the manifestation of side effects.
Scientific References
- Deciphering the selective androgen receptor modulators paradigm — Review
- Selective Androgen Receptor Modulators (LiverTox) — Review
- Considerations, possible contraindications, and potential mechanisms for deleterious effect in recreational and athletic use of SARMs: a narrative review — Review
- Selective androgen receptor modulators: an update on preclinical and clinical development — Review
- Selective androgen receptor modulators for osteoporosis and sarcopenia: preclinical rationale and translational endpoints — Review
- Selective androgen receptor modulators: clinical utility and mechanisms (overview) — Review
- Androgen receptor signaling in skeletal muscle and bone: implications for anabolic-biased modulation — Review
- Androgens and bone: cellular mechanisms and musculoskeletal remodeling endpoints — Review
- Monitoring of selective androgen receptor modulators in dietary supplements and related analytical workflows — In vitro
- Selective Androgen Receptor Modulators (SARMs): effects on performance/body and safety profile (systematic review) — Review
Cautions
- For educational and scientific context only; not intended to diagnose, treat, cure, or prevent any disease.
- If you are pregnant, nursing, have a medical condition, or use prescription medication, consult a qualified professional.
- Discontinue use if sensitivity occurs.
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ACP-105 | Pen
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