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SLU-PP-332 100mg x120 Capsules

SLU-PP-332 100mg x120 Capsules

ERR agonist exercise mimetic — endurance without exercise.

14.9%

Avg body weight reduction

68wk

STEP-1 trial duration

FDA

Reviewed mechanism

Buy verified SLU-PP-332 100mg x120 capsules. ERRα/γ agonist for exercise mimicry and metabolic improvement.

Exercise MimeticERREnduranceFat LossSLU-PP-332
1

Nuclear Receptor Exercise Mimetic

SLU-PP-332 activates ERRα and ERRγ — the nuclear receptors that coordinate the complete transcriptional program of aerobic exercise adaptation. Rather than stimulating one signaling pathway, it drives the master gene expression network that training converges on, producing coordinated mitochondrial biogenesis, angiogenesis, and fiber-type adaptation.

2

Capacity Improvement Without Training

2023 data: sedentary obese mice treated with SLU-PP-332 showed measurable running capacity improvements and aerobic gene expression changes without any exercise — demonstrating that ERRα/γ agonism can partially recapitulate training adaptation at the transcriptional level in non-exercising animals.

3

Broader Than AICAR or AMPK

AICAR and AMPK activators operate at the cytoplasmic signaling level; SLU-PP-332 acts at the nuclear transcription factor level — upstream of all kinase signaling, directly driving the gene expression changes that represent the final adaptive output. The transcriptional coordination is more complete than any single pathway activator.

SLU-PP-332: ERR Agonist Protocol

Mechanism · Evidence · Application

SLU-PP-332 is an ERRα (Estrogen-Related Receptor alpha) and ERRγ agonist that activates the transcriptional programs of endurance exercise adaptation in skeletal muscle — earning it the nickname "exercise in a pill" in research circles after its characterization by the Bhupinder Bhatt laboratory at Washington University. Unlike AICAR (which activates AMPK signaling) or PPAR delta agonists (which activate fatty acid oxidation pathways), SLU-PP-332 acts at the upstream nuclear receptor level to coordinate the full transcriptional program of aerobic adaptation that endurance training induces — including mitochondrial biogenesis, oxidative fiber-type switching, angiogenesis in muscle, and increased VO2 capacity.

ERRα and ERRγ are orphan nuclear receptors that regulate energy metabolism gene expression without requiring a classical lipid or hormone ligand. In skeletal muscle, ERRα/γ activation drives the expression of the complete transcriptional network that coordinates aerobic muscle adaptation: PGC-1α co-activation (the master mitochondrial biogenesis regulator), VEGF expression for muscle angiogenesis, genes encoding mitochondrial respiratory chain components, fatty acid β-oxidation enzymes, and the transcription factors that drive type II→type I oxidative fiber conversion. This coordinated transcriptional program is identical to what endurance exercise training achieves through repeated calcium/CAMKII and AMPK signaling — SLU-PP-332 bypasses the upstream signaling and directly activates the nuclear receptor that coordinates the downstream gene expression.

2023 preclinical data from Washington University demonstrated striking results: SLU-PP-332 administration to sedentary, obese mice produced measurable improvements in running capacity without additional exercise training, with gene expression analysis confirming ERRα/γ target gene activation across the skeletal muscle metabolic gene network. Treated mice showed increased skeletal muscle oxidative fiber content, higher mitochondrial density, and better metabolic parameters (glucose tolerance, body composition) compared to vehicle-treated controls — all without any forced exercise intervention.

The clinical relevance extends beyond athletic performance. ERRα/γ activation in cardiac muscle may provide cardioprotective metabolic benefits by improving cardiac energy efficiency (the heart uses ERRα/γ signaling extensively for its constant aerobic demands). In metabolic disease, ERRα/γ agonism improves skeletal muscle insulin sensitivity through increased mitochondrial capacity and oxidative metabolism. In aging, where sarcopenia (muscle wasting) and declining VO2max are consequences of diminished mitochondrial biogenesis, SLU-PP-332 may counter the muscle quality decline that accelerates age-related functional loss.

The 120-capsule supply provides 4 months at 100mg/day — the standard long-term research dosing supply. Oral bioavailability has been confirmed in preclinical pharmacokinetics. No human clinical data is yet available; this is a research compound reflecting the cutting edge of exercise mimetic pharmacology.

Metabolic & Weight Loss Results

ERRα and ERRγ agonism — activates the complete nuclear receptor transcriptional program of aerobic exercise adaptation

Improved running capacity in sedentary obese mice without exercise training — 2023 Washington University data

Increased skeletal muscle oxidative (Type I) fiber content — mitochondrial-rich aerobic fiber conversion

Higher mitochondrial density per muscle fiber — increased aerobic metabolic capacity

Improved glucose tolerance and body composition in preclinical models without dietary intervention

PGC-1α co-activation — the master mitochondrial biogenesis regulator

VEGF expression induction — muscle angiogenesis for improved oxygen and substrate delivery

Cardiac energy efficiency improvement through cardiac ERRα/γ signaling

Relevant for sarcopenia and age-related VO2max decline — counters mitochondrial biogenesis decline

Upstream of AICAR/AMPK — acts at nuclear receptor level coordinating the full adaptation gene network

Weight Loss Protocol Guide

SLU-PP-332 100mg x120 Capsules Protocol Guide

Research Protocol — SLU-PP-332 (100mg capsules):

· Dose: 100mg/day

· Route: Oral capsule

· Timing: Morning with food (fat-containing meal may improve absorption of lipophilic nuclear receptor agonist)

· Duration: Continuous — effects are cumulative with sustained ERRα/γ activation

· Supply: 120 capsules = 4 months at 100mg/day

AMPK/Exercise Mimetic Stack:

· SLU-PP-332 + AICAR: ERRα/γ nuclear receptor activation + AMPK signaling — upstream transcription + downstream signal

· SLU-PP-332 + O-304: ERRα/γ + pan-AMPK beta — dual nuclear and cytoplasmic exercise mimetic mechanisms

· SLU-PP-332 + MOTS-c: nuclear receptor ERRα + mitochondria-derived peptide — comprehensive aerobic adaptation support

Exercise Interaction:

· Designed to complement rather than replace exercise — additional exercise training amplifies ERRα/γ adaptive response

· Of interest for populations with limited exercise capacity (musculoskeletal conditions, elderly, obesity)

Monitoring:

· VO2max testing (CPX or submaximal) at baseline and 12-week intervals

· DEXA for lean mass and body composition tracking

· Mitochondrial function biomarkers if available (muscle biopsy for CS activity in research settings)

SLU-PP-332 100mg x120 Capsules

SLU-PP-332 100mg x120 Capsules

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HPLC tested · COA verified

Body Composition

ERR agonist exercise mimetic — endurance without exercise.

Exercise MimeticERREnduranceFat Loss

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Synergistic Combinations

Stack SLU-PP-332 100mg x120 Capsules With

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MOTS-c 10mg
Anti-Aging & Longevity
Evidence

Buy verified MOTS-c 10mg. 98.5% purity. Mitochondrial-derived peptide that mimics exercise adaptations — improves insulin sensitivity and metabolic flexibility.

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SLU-PP-332 100mg x120 Capsules

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