PEPS MN / МЭДЛЭГИЙН САН

SLU-PP-332 (Дасгалын нөлөөг дуурайх бодис)

SLU-PP-332 (Exercise Mimetic)

Synthetic Pan-ERR Agonist | Exercise Mimetic & Metabolic Modulator

Weight: 290.32 Da

Half-life: Under investigation (no human PK data)

Chain: Non-peptide small molecule

4 studies

2024 latest

2 recent

Emerging

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Groundbreaking synthetic compound from Saint Louis University functioning as pan-estrogen-related receptor agonist with preferential ERRα activity. Activates metabolic pathways engaged during physical exercise without physical activity requirement.

Mechanism of Action

Binds and activates ERRα/β/γ which regulate energy metabolism gene expression. Upregulates PGC-1α (mitochondrial biogenesis master regulator), activates AMPK pathway, increases mitochondrial density to 1.8-fold, enhances oxidative phosphorylation and ATP production.

01 Exercise mimetic effects without physical activity

02 12% weight loss in 28 days

03 70% increased endurance

04 25% enhanced fatty acid oxidation

05 Improved insulin sensitivity

06 Reduced hepatic steatosis

07 Cardiac protection

08 Reversal of age-related mitochondrial dysfunction

Molecular Data

Molecular Weight

290.32 Da

Chain Length

Non-peptide small molecule

Type

Synthetic ERR agonist

Amino Acid Sequence

(E)-4-Hydroxy-N'-(naphthalen-2-ylmethylene)benzohydrazide

Complex or non-standard sequence format

Research Indications

Metabolic Health

Weight Loss & Body Composition most effective

12% body weight reduction in 28 days without appetite suppression. Fat mass gain <0.5g vs ~5g controls.

Insulin Sensitivity & Glucose Control most effective

Significantly improved glucose tolerance in obese mice with lower fasting glucose and insulin levels.

Energy Expenditure Enhancement most effective

Increases resting energy expenditure by 25% for fatty acid oxidation within 2 hours.

Liver Health & NAFLD most effective

Reduced hepatic steatosis, decreased hepatic triglycerides, and enhanced hepatic fatty acid oxidation.

Exercise Performance

Endurance Improvements effective

70% increase in running time and 45% increase in running distance in preclinical models.

Muscle Fiber Remodeling effective

Increased type IIa oxidative skeletal muscle fibers with enhanced oxidative capacity.

Cardiovascular

Cardiac Function Improvement moderate

Improved ejection fraction in heart failure models with reduced cardiac fibrosis.

Anti-Aging

Mitochondrial Aging Reversal moderate

First compound to reverse age-related mitochondrial dysfunction in 21-month-old mice.

Kidney Protection

Age-Related Kidney Disease moderate

Reversed age-related albuminuria increase and prevented podocyte loss in elderly mice.

Dosing Protocols

Research compound – IP injection in animals only. No human administration protocols established.

Goal	Dose	Frequency	Route
Standard Metabolic Protocol	50 mg/kg (animal dosing)	Twice daily	Intraperitoneal injection (IP)
Acute Exercise Enhancement	50 mg/kg (animal dosing)	Single dose 1 hour pre-exercise	Intraperitoneal injection (IP)
Extended Treatment	50 mg/kg (animal dosing)	Twice daily for 4-8 weeks	Intraperitoneal injection (IP)

Reconstitution Instructions

Materials Needed:

Bacteriostatic water (BAC) required
Sterile technique essential

1 WARNING: Not tested in humans – research only
2 Do NOT use outside approved research protocols
3 Dosing cannot be extrapolated from animals to humans
4 No human clinical trials initiated as of 2025
5 Oral formulation in development
6 Consult medical professionals before experimental use

Interactions

Metformin

Both affect mitochondrial function and AMPK pathways – may have additive metabolic effects. Monitor blood glucose closely.

monitor

Insulin

Enhanced insulin sensitivity may require significant dose reduction to prevent hypoglycemia.

monitor

Tirzepatide

Different mechanisms affecting weight loss and metabolism – combination could have additive effects.

monitor

Semaglutide

Combining GLP-1 and ERR agonism may enhance metabolic effects – monitor weight loss rate closely.

monitor

5-Amino-1MQ

Distinct mechanisms (ERR agonism vs NNMT inhibition) likely complementary without known interactions.

compatible

NAD+

Complementary mitochondrial pathways – SLU-PP-332 increases biogenesis while NAD+ supports energy production.

synergistic

CJC-1295

GH optimization may complement metabolic enhancement for body composition without known interactions.

compatible

Ipamorelin

May preserve lean muscle during SLU-PP-332-induced fat loss through GH pathway.

compatible

What to Expect

Hours 1-6

Metabolic shift toward fat oxidation within 2 hours; gene expression changes at 3-6 hours; enhanced exercise performance 1 hour post-dose

Week 1

Increased resting energy expenditure measurable; enhanced fatty acid oxidation by 25%; improved grip strength by day 6

Week 2-4

Up to 12% weight loss by day 28; dramatic fat mass reduction; improved glucose tolerance; 45-70% endurance improvements; reduced hepatic steatosis

Week 6-8

Cardiac improvements (ejection fraction, reduced fibrosis); age-related kidney dysfunction reversal; mitochondrial architecture restoration

Long-term (5+ months)

Sustained anti-aging effects in aging studies; continued tissue mitochondrial improvement; duration after discontinuation unknown

Side Effects & Safety

Common Side Effects

Animal studies show favorable safety with no severe effects at therapeutic doses
Well-tolerated in rodents and canines
No liver, kidney, or cardiac toxicity documented
No lean mass loss
Does not suppress hormones or act as stimulant
Minor plasma cholesterol and liver enzyme changes in some studies

Stop Signs – Discontinue if:

Severe hypoglycemia (especially with diabetes medications)
Any cardiovascular symptoms (chest pain, palpitations, shortness of breath)
Signs of liver dysfunction (jaundice, dark urine, severe abdominal pain)
Kidney problems (reduced urination, swelling, severe back pain)
Severe headaches or neurological symptoms
Allergic reactions (rash, hives, difficulty breathing, swelling)

Contraindications

NOT FOR HUMAN USE – no approved human dose
No human clinical trials conducted
Potential interaction with diabetes medications

Quality Checklist

Good Signs

Legitimate research supplier with Certificate of Analysis
From reputable chemical suppliers (Cayman Chemical, Sigma-Aldrich)
Proper labeling as ‘Research Use Only’
Batch numbers and purity data (typically >98%)

Warning Signs

Research chemical only – NOT FOR HUMAN USE
NOT FDA approved – no human clinical trials
Available only for legitimate research through licensed suppliers

Bad Signs

Any product marketed for human consumption is illegal
Unknown purity or contamination without lab testing
Lack of proper HPLC or mass spectrometry verification
Products without ‘Research Use Only’ labeling

Frequently Asked Questions

Is SLU-PP-332 an actual exercise substitute, or does it just feel like you worked out?

SLU-PP-332 activates the same metabolic pathways exercise does (mitochondrial biogenesis, PGC-1α upregulation, AMPK activation), but it’s not a complete substitute. It increases endurance 70% and reduces weight 12% without exercise, but it doesn’t build muscles or improve cardiovascular fitness like real training does. Think of it as metabolic enhancement, not exercise replacement.

Why does SLU-PP-332 work so much faster than training (12% weight loss in 28 days)?

Training requires weeks to upregulate mitochondrial genes; SLU-PP-332 activates them within hours. In mouse studies, energy expenditure increased 25% within 2 hours, creating sustained fat oxidation and rapid weight loss. This bypass of normal training adaptation pathways explains the speed, though long-term human data doesn’t exist.

Could SLU-PP-332 cause liver damage if used long-term?

The file flags SLU-PP-332 as potentially hepatotoxic. However, animal studies showed no liver damage at therapeutic doses. The flag exists because long-term human safety is unknown. If used experimentally, liver function tests (ALT, AST, bilirubin) should be monitored regularly.

Is there an oral version of SLU-PP-332 in development?

Yes. SLU-PP-915 (a distinct oral bioavailable ERR pan-agonist) shows similar efficacy to SLU-PP-332 when given orally. A 2025 study found it enhanced aerobic performance as effectively as the injectable form. This represents major progress toward clinical translation, though human trials haven’t started.

References

A Synthetic ERR Agonist Alleviates Metabolic Syndrome

Billon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP

Journal of Pharmacology and Experimental Therapeutics (2024)

Diet-induced obese mice, 50 mg/kg IP twice daily, 28 days: 12% body weight loss, 25% fatty acid oxidation increase, improved glucose tolerance, reduced hepatic steatosis. SLU-PP-332 mimics exercise-induced metabolic benefits.
Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise Capacity

Billon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, Oh TG, Kazantzis M, Chatterjee A, Chrivia J et al.

ACS Chemical Biology (2023)

Multiple mouse models, 50 mg/kg IP: 70% increase in running time, 45% increase in running distance, increased type IIa oxidative muscle fibers. SLU-PP-332 is a synthetic ERR pan agonist with highest potency for ERRα.
Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging Kidney

Wang XX, Myakala K, Libby AE, Krawczyk E, Panov J, Jones BA, Bhasin K, Shults N, Qi Y, Krausz KW et al.

American Journal of Pathology (2023)

21-month-old mice, 8-week treatment with SLU-PP-332: Reversed age-related increases in albuminuria, podocyte loss, mitochondrial dysfunction, and inflammatory cytokines.
Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function

Xu W, Billon C, Li H, Wilderman A, Qi L, Graves A, Rideb JRDC, Zhao Y, Hayes M, Yu K et al.

Circulation (2024)

Both SLU-PP-332 and SLU-PP-915 significantly improved ejection fraction, ameliorated fibrosis, and increased survival in pressure overload-induced heart failure without affecting cardiac hypertrophy. Transcriptionally activated fatty acid metabolism and mitochondrial function genes.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.

PEPS MN / МЭДЛЭГИЙН САН

Erythropoietin (EPO) (EPO)

FDA Approved

EPO | Red Blood Cell Stimulating Hormone

Weight: 30,400 Da

Half-life: 4-12 hours (IV), ~25 hours (SubQ)

Chain: 165 amino acids

4 studies

2024 latest

Extensively Studied

Community Research

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Erythropoietin (EPO) is an essential glycoprotein hormone that stimulates red blood cell production. Naturally produced by the kidneys in response to low oxygen levels, recombinant human EPO is FDA-approved for treating anemia in chronic kidney disease and chemotherapy patients. EPO binding to receptors on bone marrow cells promotes survival and maturation of red blood cell precursors, increasing oxygen-carrying capacity. Due to performance-enhancing effects, it is banned in competitive sports.

Mechanism of Action

EPO binds to erythropoietin receptors (EPOR) on erythroid progenitor cells in bone marrow, activating three interconnected signaling pathways: JAK2/STAT5, PI3K/AKT, and RAS/MAPK. This promotes survival of red blood cell precursors by protecting them from apoptosis, accelerates proliferation and differentiation of erythroid cells, and increases hemoglobin production. Under hypoxic stress, endogenous EPO production can increase up to 1000-fold, demonstrating the body’s powerful oxygen-sensing regulatory system.

01 Stimulates red blood cell production

02 Increases oxygen-carrying capacity

03 FDA-approved for anemia treatment

04 Improves endurance capacity

05 Supports patients with chronic kidney disease

06 Helps chemotherapy-induced anemia

07 Well-characterized mechanism of action

08 Extensively studied safety profile

Molecular Data

Molecular Weight

30,400 Da

Chain Length

165 amino acids

Type

Glycoprotein hormone

Research Indications

Medical Indications (FDA-Approved)

CKD-Related Anemia most effective

Primary FDA-approved indication for anemia secondary to chronic kidney disease.

Chemotherapy-Induced Anemia most effective

FDA-approved for treating anemia in cancer patients receiving chemotherapy.

Surgical Blood Loss effective

Used to reduce need for blood transfusions in certain surgical settings.

Performance (Banned in Sports)

Endurance Enhancement most effective

Increases oxygen delivery to muscles, improving endurance capacity. Banned by WADA.

Altitude Acclimatization effective

May accelerate adaptation to high altitude by increasing red blood cell mass.

Dosing Protocols

EPO is administered via subcutaneous or intravenous injection. Medical use requires prescription and monitoring. Dosing is individualized based on hemoglobin levels, with targets typically kept below 11-12 g/dL to minimize cardiovascular risks.

Goal	Dose	Frequency	Route
CKD Anemia (medical)	50-100 IU/kg	3x weekly	SubQ or IV
Chemotherapy Anemia (medical)	150-300 IU/kg	3x weekly	SubQ
Maintenance (medical)	Individualized	1-3x weekly	SubQ

Reconstitution Instructions

Materials Needed:

Pre-filled syringes (most common)
Or lyophilized powder with diluent
Alcohol swabs
Cold storage

1 Most EPO comes in pre-filled syringes
2 Allow to reach room temperature before injection
3 Inject subcutaneously or intravenously as directed
4 Do not shake vials or syringes

Interactions

Iron supplementation

Iron is essential for hemoglobin production; often co-administered with EPO therapy.

synergistic

TB-500

Different mechanisms; no known interactions.

compatible

BPC-157

Different mechanisms; no known interactions.

compatible

What to Expect

Days 1-3

Bone marrow stimulation begins

Week 1-2

Reticulocyte count increases

Week 2-4

Hemoglobin begins rising

Week 4-12

Target hemoglobin achieved with proper dosing

Side Effects & Safety

Common Side Effects

Injection site reactions
Headache
Hypertension
Joint pain
Flu-like symptoms

Stop Signs – Discontinue if:

Severe headache or vision changes
Chest pain or shortness of breath
Signs of blood clots (leg swelling, pain)
Sudden loss of response to EPO

Contraindications

Uncontrolled hypertension
Pure red cell aplasia history
Hemoglobin >12 g/dL (increased cardiovascular risk)
Active malignancy (relative contraindication)

Quality Checklist

Good Signs

Clear, colorless solution
Pharmaceutical grade product
Proper cold chain maintained
Intact packaging and seals

Warning Signs

Research-grade products lack quality assurance
Temperature excursions may affect potency

Bad Signs

Cloudy or discolored solution
Particulates visible
Exposed to room temperature

Frequently Asked Questions

Why is EPO banned in sports if it’s FDA-approved as medicine?

EPO is FDA-approved specifically for anemia in kidney disease and chemotherapy patients—narrow medical indications. It’s banned in sports because it boosts oxygen delivery far beyond medical therapeutic levels, providing unfair endurance advantages. The performance-enhancing effects at doses used by athletes vastly exceed what’s used medically.

At what hemoglobin level does EPO become dangerous?

Medical guidelines recommend keeping hemoglobin below 11-12 g/dL during EPO therapy because higher levels significantly increase cardiovascular risks including blood clots, stroke, and heart attack. This ceiling exists because excessive oxygen-carrying capacity paradoxically becomes harmful, increasing blood viscosity dangerously.

Does EPO improve endurance without causing side effects?

EPO absolutely improves endurance capacity by increasing red blood cell production and oxygen delivery. However, it commonly causes water retention, joint pain, headaches, and hypertension. More concerning are thromboembolic events (blood clots) and theoretical tumor progression risk with higher doses used for performance enhancement.

How long after stopping EPO do benefits disappear?

EPO’s effects begin diminishing once injections stop as red blood cells have a natural 120-day lifespan. Hemoglobin returns toward baseline within 2-3 weeks of discontinuation. Most performance benefits fade quickly, making continued use necessary for sustained effects, which is why athletes faced testing challenges in endurance sports.

References

Erythropoietin regulation of red blood cell production

PMC/NCBI (2020)

Comprehensive review of EPO’s oxygen-sensing mechanism and regulation of RBC production.
Erythropoietin Stimulating Agents

StatPearls (NCBI Bookshelf) (2024)

FDA-approved indications include CKD anemia and chemotherapy-induced anemia. Risks increase when hemoglobin exceeds 11-12 g/dL.
Erythropoiesis-stimulating agents and other methods to enhance oxygen transport

PMC (2008)

rHuEPO increases O2 supply to muscles and boosts performance in endurance sports.
The mechanism of erythropoietin action

PubMed (1992)

EPO promotes survival of erythroid progenitors by protecting from apoptosis.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.

PEPS MN / МЭДЛЭГИЙН САН

L-Carnitine (Levocarnitine)

FDA Approved

Amino Acid Derivative | Fatty Acid Transporter

Weight: 161.20 Da

Half-life: ~2-3 hours (injectable)

2 studies

2018 latest

established

Community Research

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L-Carnitine is an amino acid derivative naturally produced in the body and essential for transporting long-chain fatty acids into mitochondria for energy production. Injectable forms bypass digestive absorption limitations of oral supplements.

Mechanism of Action

Acts as a carrier molecule, shuttling long-chain fatty acids across the inner mitochondrial membrane via the carnitine palmitoyltransferase (CPT) system. This is the rate-limiting step in fatty acid oxidation for energy production.

01 Enhanced fatty acid transport to mitochondria

02 Improved energy production from fats

03 Better bioavailability than oral forms

04 Support for exercise recovery

05 Potential cognitive benefits

Molecular Data

Molecular Weight

161.20 Da

Type

Quaternary ammonium compound

Research Indications

Metabolic

Fatty Acid Oxidation most effective

Primary function transporting fatty acids into mitochondria for beta-oxidation.

Energy Production effective

Supports ATP generation from fat metabolism, particularly during exercise.

Weight Management moderate

May enhance fat utilization when combined with exercise and caloric deficit.

Performance

Exercise Recovery moderate

May reduce muscle damage markers and improve recovery post-exercise.

Endurance Support moderate

Enhances fat utilization during prolonged exercise, potentially sparing glycogen.

Clinical Uses

Carnitine Deficiency most effective

FDA-approved treatment for primary and secondary carnitine deficiency.

Dialysis Support effective

Used in patients on hemodialysis who develop carnitine depletion.

Dosing Protocols

Subcutaneous or intramuscular injection provides superior bioavailability compared to oral supplementation, which is limited to ~15-20% absorption.

Goal	Dose	Frequency	Route
Standard Protocol	50-100mg	Daily	SubQ
Advanced Protocol	100-200mg	Daily	SubQ or IM
Pre-Workout	100-200mg	30-60 min before exercise	SubQ

Reconstitution Instructions

Materials Needed:

L-Carnitine lyophilized powder (typically 200mg vial)
Bacteriostatic water (2.0mL recommended)
Insulin syringes (29-31 gauge)
Alcohol swabs

1 Allow vial to reach room temperature
2 Clean rubber stopper with alcohol swab
3 Add 2.0mL bacteriostatic water for 100mg/mL concentration
4 Inject slowly along vial wall
5 Gently swirl to dissolve; never shake
6 Label with date and store refrigerated at 2-8°C
7 Use within 2-4 weeks of reconstitution

Interactions

Thyroid Hormones

L-Carnitine may affect thyroid hormone action. Those on thyroid medication should monitor levels.

monitor

Anticoagulants

May enhance effects of warfarin and similar medications.

monitor

What to Expect

Immediate

Injectable form provides rapid absorption within 30-60 minutes

Week 1-2

Potential improvements in energy and exercise capacity

Week 4-8

Cumulative benefits on fat metabolism and recovery

Week 8-16

Full metabolic optimization when combined with exercise

Side Effects & Safety

Common Side Effects

Injection site reactions
Mild nausea
Body odor (fishy smell at high doses)

Stop Signs – Discontinue if:

Allergic reactions (rare)
Severe gastrointestinal distress
Unusual muscle weakness

Contraindications

Seizure disorders (may lower seizure threshold)
Hypothyroidism (may affect thyroid function)
Allergy to carnitine products

Quality Checklist

Good Signs

White crystalline powder
Clear, colorless solution after reconstitution
Certificate of Analysis with purity testing

Warning Signs

Should dissolve completely without residue

Bad Signs

Discolored powder
Cloudy or particulate solution
Strong unusual odor

Frequently Asked Questions

Why inject L-carnitine when oral supplements are available?

Oral L-carnitine has only 15-20% bioavailability due to poor intestinal absorption. Injectable forms achieve near 100% bioavailability, delivering much higher effective doses directly into circulation. Injectable is significantly more efficient if cost and needle anxiety aren’t factors.

Does L-carnitine actually help fat loss?

L-carnitine enhances fatty acid transport into mitochondria for energy production. It works best when combined with exercise and caloric deficit. Modest benefits (5-10% improvements in fat loss) are most visible in well-trained athletes or those with pre-existing carnitine deficiency.

Can I take L-carnitine before cardio?

Yes. Injecting 100-200mg 30-60 minutes before endurance exercise optimizes fatty acid utilization and may improve performance slightly. Time it to maximize fat-burning potential, though benefits are most apparent during prolonged low-to-moderate intensity work.

Will L-carnitine affect thyroid function?

L-carnitine may affect thyroid hormone action in some individuals. If you’re on thyroid medication (T3/T4), monitor thyroid levels before and after starting carnitine supplementation. Adjustments to thyroid dosing may be necessary in some cases.

References

L-Carnitine Supplementation and Exercise

(2018)

Meta-analysis showing modest benefits of L-carnitine on exercise performance and recovery markers.
Carnitine Metabolism and Function

(2012)

Comprehensive review of carnitine’s role in fatty acid transport and energy metabolism.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.

PEPS MN / МЭДЛЭГИЙН САН

AICAR (Acadesine)

5-Aminoimidazole-4-carboxamide Ribonucleotide | AMPK Activator

Weight: 338.21 Da

Half-life: ~2-3 hours

2 studies

2012 latest

limited

Community Research

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AICAR is a cell-permeable nucleoside analog that activates AMP-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis. Originally studied for cardiac ischemia protection, it gained attention as an ‘exercise mimetic’ due to its metabolic effects.

Mechanism of Action

Once inside cells, AICAR is phosphorylated to ZMP, which mimics AMP and activates AMPK. This triggers metabolic pathways typically activated during exercise: increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis.

01 AMPK pathway activation

02 Enhanced fatty acid oxidation

03 Improved glucose uptake

04 Potential endurance enhancement

05 Mitochondrial biogenesis stimulation

Molecular Data

Molecular Weight

338.21 Da

Type

Nucleoside analog

Research Indications

Metabolic

AMPK Activation most effective

Directly activates the master metabolic regulator through ZMP accumulation.

Fatty Acid Oxidation effective

Increases fat burning through AMPK-mediated pathways.

Glucose Metabolism effective

Enhances glucose uptake independent of insulin in some tissues.

Performance

Endurance Enhancement moderate

Animal studies showed increased running endurance; human data limited.

Mitochondrial Biogenesis moderate

AMPK activation promotes new mitochondria formation over time.

Cardioprotection

Ischemia Protection moderate

Original clinical interest; may protect heart tissue during reduced blood flow.

Dosing Protocols

Subcutaneous injection once daily. Progressive dosing protocols are common to assess tolerance.

Goal	Dose	Frequency	Route
Standard Protocol	1-3mg	Daily	SubQ
Gradual Introduction	1mg → 2mg → 3mg	Daily, titrating over 4 weeks	SubQ
Advanced Protocol	3-5mg	Daily for 8-12 weeks	SubQ

Reconstitution Instructions

Materials Needed:

AICAR lyophilized powder (typically 50mg vial)
Bacteriostatic water (3.0mL recommended)
Insulin syringes (29-31 gauge)
Alcohol swabs

1 Allow vial to reach room temperature
2 Clean rubber stopper with alcohol swab
3 Add 3.0mL bacteriostatic water for ~16.7mg/mL concentration
4 Inject slowly along vial wall to avoid foaming
5 Gently swirl to dissolve; never shake
6 Label with date and store refrigerated at 2-8°C
7 Use within 4 weeks of reconstitution

Interactions

Metformin

Both activate AMPK through different mechanisms. Combined use may have additive effects on glucose metabolism.

monitor

GW501516

Different pathways (AMPK vs PPARδ) that may complement metabolic effects. Popular research combination.

synergistic

SR9009

Rev-ErbA agonist with complementary metabolic effects.

synergistic

What to Expect

Week 1-2

Subtle changes in energy levels; body adjusting to AMPK activation

Week 3-4

Potential improvements in endurance capacity and metabolic markers

Week 5-8

Cumulative metabolic adaptations; enhanced fat oxidation

Week 8-12

Full effects on mitochondrial density and metabolic efficiency

Side Effects & Safety

Common Side Effects

Injection site reactions
Mild fatigue during adaptation
Potential hypoglycemia

Stop Signs – Discontinue if:

Severe hypoglycemia symptoms
Lactic acidosis symptoms (muscle pain, weakness, difficulty breathing)
Unusual cardiac symptoms
Severe fatigue or weakness

Contraindications

Diabetes (risk of hypoglycemia)
Cardiac conditions
Pregnancy or breastfeeding
Competitive athletes (WADA prohibited)

Quality Checklist

Good Signs

White to off-white lyophilized powder
Clear solution after reconstitution
Certificate of Analysis with purity testing

Warning Signs

Slight yellowing may occur but should dissolve clearly

Bad Signs

Discolored or clumped powder
Cloudy solution after reconstitution
Particulate matter visible

Frequently Asked Questions

Does AICAR actually work as an ‘exercise mimetic’ in humans?

Animal studies show AICAR increased running endurance by 44% without training. However, this was mice, not humans. Humans have never been adequately tested for AICAR’s endurance effects, so calling it an exercise mimetic is speculative. The compound does activate AMPK and increase fat oxidation, but real-world performance gains in people are unproven.

Is AICAR banned in sports and why?

Yes, AICAR is WADA prohibited. While it’s not anabolic per se, it provides competitive advantage through enhanced metabolic efficiency and endurance. Athletes competing under WADA rules must avoid it entirely due to testing likelihood and strict liability regulations.

What’s the risk of hypoglycemia on AICAR if I’m not diabetic?

AICAR increases glucose uptake independent of insulin in some tissues, creating theoretical hypoglycemia risk especially in non-diabetics with normal insulin sensitivity. Diabetics face more serious risk, which is why AICAR is contraindicated in diabetes. Monitor blood glucose closely, particularly during initial doses.

How does AICAR differ from GW501516 for metabolic enhancement?

AICAR activates AMPK, the master metabolic regulator, increasing fatty acid oxidation and glucose uptake. GW501516 is a PPARδ agonist with different downstream effects. They’re often stacked because they target complementary pathways—AMPK plus PPARδ activation produces synergistic metabolic effects.

References

AMPK and Exercise: Glucose Uptake and Insulin Sensitivity

(2012)

Review of AMPK role in exercise-induced metabolic adaptations and AICAR as pharmacological activator.
AICAR Mouse Endurance Study

(2008)

Mice treated with AICAR showed 44% increase in running endurance without training.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.

SLU-PP-332 (Дасгалын нөлөөг дуурайх бодис)

SLU-PP-332 (Exercise Mimetic)

Community Research

Molecular Data

Research Indications

Dosing Protocols

Reconstitution Instructions

Interactions

What to Expect

Side Effects & Safety

Common Side Effects

Stop Signs – Discontinue if:

Contraindications

Quality Checklist

Good Signs

Warning Signs

Bad Signs

Frequently Asked Questions

Is SLU-PP-332 an actual exercise substitute, or does it just feel like you worked out?

Why does SLU-PP-332 work so much faster than training (12% weight loss in 28 days)?

Could SLU-PP-332 cause liver damage if used long-term?

Is there an oral version of SLU-PP-332 in development?

References

Related Peptides

Disclaimer

Erythropoietin (EPO) (EPO)

Erythropoietin (EPO) (EPO)

Community Research

Molecular Data

Research Indications

Dosing Protocols

Reconstitution Instructions

Interactions

What to Expect

Side Effects & Safety

Common Side Effects

Stop Signs – Discontinue if:

Contraindications

Quality Checklist

Good Signs

Warning Signs

Bad Signs

Frequently Asked Questions

Why is EPO banned in sports if it’s FDA-approved as medicine?

At what hemoglobin level does EPO become dangerous?

Does EPO improve endurance without causing side effects?

How long after stopping EPO do benefits disappear?

References

Related Peptides

Disclaimer

L-Carnitine (Levocarnitine)

L-Carnitine (Levocarnitine)

Community Research

Molecular Data

Research Indications

Dosing Protocols

Reconstitution Instructions

Interactions

What to Expect

Side Effects & Safety

Common Side Effects

Stop Signs – Discontinue if:

Contraindications

Quality Checklist

Good Signs

Warning Signs

Bad Signs

Frequently Asked Questions

Why inject L-carnitine when oral supplements are available?

Does L-carnitine actually help fat loss?

Can I take L-carnitine before cardio?

Will L-carnitine affect thyroid function?

References

Disclaimer

AICAR (Acadesine)

AICAR (Acadesine)

Community Research

Molecular Data

Research Indications

Dosing Protocols