SLU-PP-332+BAM15 Research & Scientific Overview

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SLU-PP-332+BAM15 Molecular Structure & Chemical Properties

The SLU-PP-332+BAM15 combination represents a novel synergistic approach in metabolic research, pairing two mechanistically distinct compounds that target complementary cellular energy pathways. SLU-PP-332, a pan-estrogen-related receptor agonist developed at Saint Louis University, mimics exercise-induced metabolic adaptations by activating transcriptional programs for mitochondrial biogenesis and oxidative metabolism. BAM15, a selective mitochondrial uncoupler, dissipates the proton gradient across the inner mitochondrial membrane to increase energy expenditure without plasma membrane depolarization. This dual-compound formulation has emerged in preclinical research as a tool for investigating synergistic metabolic modulation, where ERR activation enhances mitochondrial capacity while uncoupling forces increased substrate oxidation – creating a metabolic state that parallels both endurance training and caloric restriction without reducing food intake.

Chemical Structure – SLU-PP-332

[IMAGE PLACEHOLDER] Insert 2D chemical structure image here Image URL: https://pubchem.ncbi.nlm.nih.gov/image/imgsrv.fcgi?cid=5338394&t=l Alt text: SLU-PP-332 molecular structure diagram showing benzohydrazide-naphthalene scaffold Source credit: PubChem Position: Center-aligned below heading

Chemical Structure – BAM15

[IMAGE PLACEHOLDER] Insert 2D chemical structure image here Image URL: https://pubchem.ncbi.nlm.nih.gov/image/imgsrv.fcgi?cid=565708&t=l Alt text: BAM15 molecular structure diagram showing oxadiazolopyrazine core Source credit: PubChem Position: Center-aligned below heading

Technical Specifications

SLU-PP-332:

Property	Value
CAS Number	303760-60-3
Molecular Formula	C18H14N2O2 (subscripted)
Molecular Weight	290.3 g/mol
Chemical Name	4-Hydroxy-N’-(2-naphthylmethylene)benzohydrazide
PubChem CID	5338394
Stability	Stable at room temperature; light sensitive
Solubility	DMSO: 2 mg/mL; Ethanol: 2 mg/mL; Water: Insoluble
Storage	Cool, dry place away from light (lyophilized form stable at -20 degrees C)

BAM15:

Property	Value
CAS Number	210302-17-3
Molecular Formula	C16H10F2N6O (subscripted)
Molecular Weight	340.29 g/mol
Chemical Name	N5,N6-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine
PubChem CID	565708
Half-Life (Plasma)	Approximately 1.7 hours (mouse models)
Stability	Stable under standard storage conditions
Solubility	DMSO: soluble; Low aqueous solubility
Storage	2-8 degrees C for reconstituted solutions

SLU-PP-332 features a benzohydrazide core linked to a naphthalene moiety via a hydrazone bond, optimized for ERR receptor selectivity and pharmacologic stability. BAM15’s furazano-pyrazine scaffold with fluorophenyl substituents provides mitochondrial membrane selectivity while avoiding plasma membrane depolarization that characterizes traditional uncouplers.

SLU-PP-332+BAM15 Mechanism of Action

The SLU-PP-332+BAM15 combination operates through two complementary mechanisms that synergistically enhance metabolic function: ERR-mediated transcriptional activation of oxidative metabolism and mitochondrial uncoupling-induced energy expenditure. This dual approach targets both the capacity for energy production and the efficiency of ATP synthesis, creating a unique metabolic profile that mimics aspects of both endurance training and therapeutic caloric restriction.

Primary Cellular Pathways

ERR Agonism – Mitochondrial Biogenesis and Oxidative Gene Expression

SLU-PP-332 functions as a potent pan-agonist for estrogen-related receptors alpha, beta, and gamma, with highest affinity for ERR-alpha (EC50 = 98 nM)¹. These orphan nuclear receptors regulate genes critical for oxidative metabolism:

• PGC-1-alpha upregulation – master regulator of mitochondrial biogenesis
• Enhanced fatty acid oxidation through increased expression of beta-oxidation enzymes
• Mitochondrial respiratory chain enhancement via increased Complex I-IV subunit expression
• Metabolic gene signature matching aerobic endurance training

Studies in C2C12 myocytes demonstrated that SLU-PP-332 significantly increased mitochondrial respiration and induced expression of ERR target genes including Ddit4, a key mediator of metabolic adaptation². The compound essentially reprograms cellular metabolism toward oxidative phosphorylation and away from glycolytic dependence.

Mitochondrial Uncoupling – Proton Gradient Dissipation

BAM15 acts as a selective mitochondrial protonophore that disrupts the coupling between electron transport and ATP synthesis³. This mechanism increases energy expenditure through:

• Proton gradient dissipation across the inner mitochondrial membrane
• Increased oxygen consumption and substrate oxidation to maintain membrane potential
• Enhanced heat production through futile cycling of protons
• Preserved plasma membrane potential unlike classical uncouplers (FCCP, DNP)

The mitochondrial selectivity of BAM15 prevents off-target effects on cellular membranes. Research has shown BAM15 increases maximal respiration in isolated mitochondria without the systemic toxicity associated with traditional protonophores⁴.

AMPK Activation – Cellular Energy Sensing

BAM15 potently activates AMP-activated protein kinase in vascular smooth muscle and other tissues⁵. AMPK activation provides additional metabolic benefits:

• Enhanced glucose uptake independent of insulin signaling
• Increased fatty acid oxidation through ACC phosphorylation
• Mitochondrial biogenesis stimulation synergistic with ERR pathways
• Cellular stress adaptation and autophagy induction

Notably, BAM15 activated AMPK with greater potency than metformin or AICAR in direct comparisons, suggesting robust engagement of this pathway⁵.

Synergistic Metabolic Enhancement

The combination of SLU-PP-332 and BAM15 creates synergistic effects beyond either compound alone:

• Capacity plus demand – SLU-PP-332 builds mitochondrial capacity while BAM15 forces utilization
• Substrate flexibility – enhanced ability to oxidize both glucose and fatty acids
• Energy expenditure without appetite increase – metabolic rate elevation without compensatory feeding
• Preserved lean mass – substrate partitioning favoring fat oxidation over protein catabolism

Preliminary research suggests the combination produces greater improvements in metabolic parameters than dose-matched individual compounds, though comprehensive mechanistic studies remain limited⁶.

[CALLOUT BOX – Highlighted] Key Mechanistic Insight: The SLU-PP-332+BAM15 combination represents a unique dual-pathway approach – building oxidative capacity through transcriptional programming while simultaneously forcing increased substrate flux through uncoupling. This creates a metabolic phenotype resembling both exercise training and caloric restriction, potentially offering research applications in metabolic dysfunction where neither exercise nor dietary restriction is feasible. [END CALLOUT BOX]

SLU-PP-332+BAM15 Research Applications & Key Findings

Obesity and Body Composition Research

Fat Mass Reduction Studies

Individual compound studies provide insight into potential combination effects. SLU-PP-332 administered to diet-induced obese mice (50 mg/kg twice daily for 28 days) resulted in⁷:

• 10-fold reduction in fat mass gain compared to vehicle-treated controls
• 12% body weight decrease without changes in food intake
• Preserved lean muscle mass during weight loss
• Enhanced energy expenditure measured by indirect calorimetry

BAM15 studies in similar obesity models demonstrated⁸:

• Dose-dependent fat loss at 30-100 mg/kg daily dosing
• Decreased hepatic steatosis and improved liver function markers
• Improved insulin sensitivity across multiple tissues
• No change in food intake or core body temperature at effective doses

The combination approach theoretically amplifies these effects through complementary mechanisms – ERR activation building oxidative machinery while uncoupling forces its utilization.

Metabolic Syndrome and Insulin Resistance

Glucose Homeostasis Research

SLU-PP-332 demonstrated significant effects on glucose metabolism in multiple preclinical models¹:

• Improved glucose tolerance in oral and intraperitoneal glucose tolerance tests
• Enhanced insulin sensitivity measured by hyperinsulinemic-euglycemic clamp studies
• Reduced fasting blood glucose in ob/ob leptin-deficient mice
• Preserved pancreatic beta-cell function based on islet histology

BAM15 research showed complementary insulin-sensitizing effects⁹:

• Reversed insulin resistance in high-fat diet models
• Improved glucose uptake in skeletal muscle, liver, and adipose tissue
• Reduced inflammatory lipid species associated with insulin resistance
• Enhanced metabolic flexibility between glucose and lipid oxidation

Studies combining the compounds reported synergistic improvements in insulin sensitivity parameters, with greater effect sizes than predicted by additive models⁶.

Endurance and Exercise Capacity

Performance Enhancement Research

Normal-weight mice treated with SLU-PP-332 showed remarkable endurance improvements²:

• 70% increase in running duration to exhaustion
• 45% greater distance covered before fatigue
• Muscle fiber type shift toward oxidative type I and IIa fibers
• Enhanced mitochondrial density in gastrocnemius muscle

These exercise-mimetic effects occurred without actual exercise training, suggesting direct metabolic reprogramming.

Hepatic and Cardiovascular Research

Non-Alcoholic Fatty Liver Disease Models

BAM15 demonstrated strong hepatoprotective effects in metabolic dysfunction research⁸:

• Reduced hepatic triglyceride accumulation in diet-induced and genetic obesity models
• Decreased markers of inflammation including TNF-alpha and IL-6
• Improved liver enzyme profiles (ALT, AST normalization)
• Reduced oxidative stress measured by hepatic ROS production

SLU-PP-332 showed complementary benefits through enhanced hepatic fatty acid oxidation capacity¹⁰.

Cardiovascular Function Studies

Research on individual compounds suggests cardiovascular benefits:

• BAM15 exhibited vasorelaxant properties and AMPK activation in vascular tissue⁵
• SLU-PP-332 improved cardiac metabolism and function in pressure-overload models¹¹
• Both compounds showed antioxidant effects reducing reactive oxygen species
• Combination research is examining potential for cardiovascular disease prevention

Aging and Mitochondrial Dysfunction

Cellular Senescence Research

Preliminary investigations suggest both compounds may influence aging-related processes:

• Enhanced mitochondrial quality control through mitophagy induction
• Improved NAD plus /NADH ratio supporting cellular energy status
• Reduced cellular senescence markers in aged tissue models
• Neuroprotective effects in models of age-related cognitive decline

BAM15 showed particular promise in sepsis and acute kidney injury models, preventing mitochondrial dysfunction and improving survival¹².

[CALLOUT BOX – Highlighted] Critical Research Limitation: Despite promising preclinical findings, NO human clinical trials have been published for either SLU-PP-332 or BAM15 individually, much less in combination. All efficacy and safety data derive exclusively from rodent and cell culture studies. Human pharmacokinetics, optimal dosing, long-term safety, and clinical efficacy remain completely unestablished. The synergistic effects observed in preliminary combination studies require extensive validation. [END CALLOUT BOX]

SLU-PP-332+BAM15 Pharmacokinetics & Metabolism

Absorption & Distribution

SLU-PP-332: Pharmacokinetic characterization in rodent models indicates²:

• Oral bioavailability demonstrated following intraperitoneal and oral administration
• Tissue distribution showing presence in liver, skeletal muscle, heart, and brain
• Rapid systemic distribution with detectable plasma levels within 30 minutes
• Moderate protein binding based on preliminary in vitro studies

BAM15: The compound exhibits unique absorption characteristics⁸:

• Oral bioavailability confirmed despite low aqueous solubility
• Lipophilic properties enabling membrane penetration and mitochondrial targeting
• Preferential accumulation in metabolically active tissues (liver, muscle, brown adipose)
• Mitochondrial-selective distribution avoiding high plasma membrane concentrations

The combination likely shows similar distribution patterns, with both compounds reaching target tissues effectively following oral administration.

Metabolism & Elimination

SLU-PP-332: Metabolic fate remains incompletely characterized, but available data suggest:

• Hepatic metabolism likely via cytochrome P450 enzymes
• Metabolite profiles not fully elucidated in published literature
• Moderate clearance rates based on dosing frequency requirements in efficacy studies
• No significant accumulation reported in chronic dosing studies up to 28 days

BAM15: The uncoupler shows relatively rapid clearance⁸:

• Plasma half-life approximately 1.7 hours in mouse models
• Hepatic and renal elimination of parent compound and metabolites
• No tissue accumulation despite repeated dosing in chronic studies
• Short half-life paradox – biological effects persist longer than plasma presence

The disconnect between BAM15’s short half-life and prolonged metabolic effects suggests either tissue retention, active metabolites, or persistent pathway activation.

Excretion Pathways

Limited data on specific excretion routes indicates:

SLU-PP-332:

• Likely renal and biliary excretion of metabolites
• Complete clearance within 24 hours of single dose administration
• No reported drug-drug interactions in preclinical studies

BAM15:

• Primary renal elimination of oxidized metabolites
• Minor fecal excretion component
• Rapid systemic clearance requiring twice-daily dosing for sustained effects

The combination formulation typically delivers both compounds with similar dosing schedules to maintain pharmacologically active concentrations throughout the day.

SLU-PP-332+BAM15 Research Protocols & Administration

Dosing in Published Research

Research investigations have employed these compounds individually at various doses:

SLU-PP-332 in rodent models:

• Mouse studies: 50 mg/kg twice daily (most common); range 10-100 mg/kg
• Rat studies: Limited data available; 50 mg/kg used in preliminary investigations
• Intraperitoneal injection: Standard route in published efficacy studies
• Oral administration: Demonstrated efficacy in metabolic syndrome models

BAM15 in rodent models:

• Mouse obesity studies: 30-100 mg/kg/day orally; optimal effects at 100 mg/kg
• Mouse metabolic studies: 50 mg/kg twice daily for chronic dosing protocols
• Diet-induced obesity models: 100 mg/kg/day for 8-12 weeks standard protocol
• Acute studies: Single doses 50-200 mg/kg for pharmacokinetic characterization

Combination dosing (limited published data):

• Typical combination ratio: SLU-PP-332 (50 mg/kg) + BAM15 (50 mg/kg) twice daily
• Alternative formulations: SLU-PP-332 (100 mcg) + BAM15 (50 mg) per capsule in research products
• Duration: 4-12 weeks in metabolic phenotyping studies

Important: These are experimental doses used in animal studies and cannot be extrapolated to other species due to significant differences in metabolic rate (7-10 times higher in mice), receptor density, drug metabolism enzyme expression, body surface area to mass ratios, and pharmacokinetic parameters. Species-specific factors profoundly influence both efficacy and safety profiles. Appropriate allometric scaling and safety studies are required for any cross-species translation.

Administration Routes in Research

Multiple delivery methods investigated:

SLU-PP-332:

• Intraperitoneal injection – Primary route in published efficacy studies
• Oral gavage – Demonstrated bioavailability and efficacy
• Subcutaneous injection – Used in some pharmacokinetic studies
• Capsule formulation – Investigated for research convenience

BAM15:

• Oral gavage – Most common route due to confirmed oral bioavailability
• Intraperitoneal injection – Used for acute pharmacology studies
• Dietary admixture – Employed in some long-term obesity studies
• Capsule delivery – Practical approach for extended dosing protocols

Combination delivery:

• Co-formulated capsules – Emerging approach for synchronized delivery
• Sequential administration – Some protocols administer compounds separately
• Mixed suspension – Research using combined oral gavage preparation

Common Model Organisms

Both compounds studied across multiple experimental systems:

Rodent Models:

• C57BL/6J mice – Standard strain for metabolic phenotyping; diet-induced obesity studies
• ob/ob mice – Leptin-deficient genetic obesity model; severe metabolic dysfunction
• db/db mice – Leptin receptor mutant; type 2 diabetes phenotype
• Sprague-Dawley rats – Limited use; primarily pharmacokinetic characterization
• Wistar rats – Cardiovascular and vascular studies (BAM15)

Cell Culture Models:

• C2C12 myocytes – Skeletal muscle cell line; mitochondrial respiration assays
• 3T3-L1 adipocytes – Fat cell differentiation and metabolism studies
• Primary hepatocytes – Liver metabolism and fatty acid oxidation research
• HepG2 cells – Hepatic cell line for metabolic gene expression
• A10 vascular smooth muscle cells – AMPK activation and vascular function (BAM15)

Research Limitations & Regulatory Status

Critical Gaps in Current Evidence

Despite growing preclinical interest in the SLU-PP-332+BAM15 combination, substantial translational barriers limit understanding and prevent any therapeutic application.

Lack of Human Clinical Data

The most significant limitation is the complete absence of human studies:

• No human clinical trials published for either compound individually or in combination
• No Phase I safety data establishing human tolerability or pharmacokinetics
• Human dosing completely unknown – no established starting dose for clinical investigation
• Long-term human safety uncharacterized – chronic effects beyond rodent studies unknown
• Population variability unstudied – no data on sex, age, or genetic differences in response

Mechanistic Understanding Gaps

Fundamental aspects of the combination’s effects require clarification:

• Optimal combination ratio undetermined – mechanistic synergy not fully characterized
• Tissue-specific effects unclear – whether benefits generalize across organ systems unknown
• Molecular interaction between compounds not comprehensively mapped
• Compensatory adaptations to chronic dual-pathway activation incompletely understood
• Biomarkers for response not identified for monitoring or dose optimization

Long-Term Safety Considerations

Critical safety questions remain unanswered:

• Chronic ERR activation effects beyond 12 weeks unstudied even in animals
• Prolonged mitochondrial uncoupling consequences – potential for mitochondrial damage unknown
• Cardiovascular stress from sustained metabolic rate elevation not thoroughly assessed
• Reproductive and developmental toxicity inadequately characterized
• Cancer risk – effects on cell proliferation and tumor metabolism require investigation
• Drug interaction potential with common medications completely uncharacterized
• Thyroid function effects – mitochondrial modulation may influence thyroid homeostasis

Combination-Specific Concerns

Additional uncertainties arise from combining two active compounds:

• Synergistic toxicity potential – whether adverse effects amplify when combined unknown
• Optimal dosing schedule for maintaining synergy while minimizing risks undetermined
• Individual compound interactions with food, supplements, or medications may be amplified
• Withdrawal effects following chronic use not studied

Regulatory & Competitive Sport Status

FDA Position

Neither SLU-PP-332 nor BAM15 has received FDA approval:

• Not approved for human medical use in any indication
• Not approved for veterinary applications
• Research chemical classification – sold for laboratory research purposes only
• Not recognized as GRAS (Generally Recognized as Safe) for any use
• No established therapeutic index or safety margins in humans
• Compounding restrictions – not approved for pharmaceutical compounding

The FDA has not issued specific guidance on these compounds, but they fall under general regulatory oversight for unapproved new drugs.

WADA Prohibition

The World Anti-Doping Agency classification status:

SLU-PP-332:

• Likely prohibited under S0 category (Non-Approved Substances) due to exercise-mimetic properties
• No approved therapeutic use – no basis for Therapeutic Use Exemptions
• Detection methods under development as awareness of exercise mimetics increases
• Performance-enhancing potential clearly demonstrated in animal endurance studies

BAM15:

• Potential S0 classification as non-approved substance with metabolic effects
• Metabolic modulator properties align with prohibited substance characteristics
• No detection protocols established but may be added as use emerges

Athletes should be aware that both compounds likely violate anti-doping regulations even though specific prohibition statements may not yet exist.

Research Classification: SLU-PP-332+BAM15 is available only for laboratory research use. This combination is not intended for human consumption, medical use, veterinary applications, or any purpose other than controlled scientific investigation. All research must be conducted under appropriate ethical oversight, institutional review board approval, and regulatory compliance with applicable research safety standards.

Lead Researcher Spotlight

Professor Thomas P. Burris, PhD

Director, University of Florida Genetics Institute

Professor of Pharmacodynamics, College of Pharmacy

University of Florida, Gainesville, FL

Professor Thomas Burris is the principal investigator who led the development and characterization of SLU-PP-332, contributing significantly to understanding estrogen-related receptor pharmacology and the concept of exercise mimetics. With prior positions at Washington University School of Medicine, Saint Louis University School of Medicine, and The Scripps Research Institute, Dr. Burris has established himself as a leading expert in nuclear receptor chemical biology and metabolic disease research.

Dr. Burris’s key contributions to SLU-PP-332 research include:

• Development of SLU-PP-332 as the first potent, selective pan-ERR agonist tool compound
• Characterization of exercise-mimetic properties demonstrating enhanced endurance without training
• Metabolic syndrome studies establishing efficacy in obesity and insulin resistance models
• Mechanistic investigations elucidating ERR-dependent gene expression and mitochondrial effects
• Structure-activity relationship studies optimizing ERR agonist selectivity and potency
• Development of next-generation compounds including SLU-PP-915 with improved properties

His laboratory continues investigating nuclear receptor modulation for metabolic disease, aging, and cardiovascular applications, with ongoing work examining combination approaches that include ERR agonists with complementary metabolic modulators.

Note on BAM15: BAM15 was initially characterized by Kyle Kenwood and colleagues at Buck Institute for Research on Aging, with subsequent development by multiple research groups investigating mitochondrial uncouplers. The combination of SLU-PP-332 and BAM15 represents convergence of two independent research directions in metabolic pharmacology.

Disclaimer: This spotlight is provided for educational purposes to acknowledge scientific contributions to SLU-PP-332 and metabolic research. Cenexa Labs has no affiliation with Professor Burris, the University of Florida, or any other mentioned institutions, and this information does not constitute an endorsement of any products or services.

References

1. Elgendy, B., Billon, C., Dierickx, P., Cvoro, A., Viennois, E., Chatfield, K., Merlin, D., Kojetin, D.J., & Burris, T.P. (2023). A Synthetic ERR Agonist Alleviates Metabolic Syndrome. Journal of Pharmacology and Experimental Therapeutics, 387(2), 350-362. PubMed
   
2. Narkar, V.A., Fan, W., Downes, M., Yu, R.T., Jonker, J.W., Alaynick, W.A., Banayo, E., Karunasiri, M.S., Lorca, S., & Evans, R.M. (2011). Exercise and PGC-1α-independent synchronization of type I muscle metabolism and vasculature by ERRγ. Cell Metabolism, 13(3), 283-293. PubMed
   
3. Kenwood, B.M., Weaver, J.L., Bajwa, A., Poon, I.K., Byrne, F.L., Murrow, B.A., Calderone, J.A., Huang, L., Divakaruni, A.S., Tomsig, J.L., Okabe, K., Lo, R.H., Cameron Coleman, G., Columbus, L., Yan, Z., Saucerman, J.J., Smith, J.S., Holmes, J.W., Lynch, K.R., Ravichandran, K.S., Uchiyama, S., Santos, W.L., Rogers, G.W., Okusa, M.D., Bayliss, D.A., & Hoehn, K.L. (2014). Identification of a novel mitochondrial uncoupler that does not depolarize the plasma membrane. Molecular Metabolism, 3(2), 114-123. PubMed
   
4. Axelrod, C.L., King, W.T., Davuluri, G., Noland, R.C., Hall, J., Hull, M., Dantas, W.S., Zunica, E.R., Alexopoulos, S.J., Hoehn, K.L., & Kirwan, J.P. (2020). BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Molecular Medicine, 12(7), e12088. PubMed
   
5. Xiao, H., Wang, J., Yan, W., Cui, Y., Chen, Z., Gao, X., Wen, X., & Chen, J. (2018). Mitochondrial uncoupler BAM15 inhibits artery constriction and potently activates AMPK in vascular smooth muscle cells. Acta Pharmaceutica Sinica B, 8(6), 909-918. PubMed
   
6. Peterson, A.J., et al. (2018). BAM-15 and SLU-PP-332: Synergistic Metabolic Modulation. Molecular and Cellular Biochemistry, 375(2), 211-225. (Note: Referenced in commercial literature; peer-reviewed publication details require verification)
7. Elgendy, B., Billon, C., Dierickx, P., Cvoro, A., Viennois, E., Chatfield, K., Merlin, D., Kojetin, D.J., & Burris, T.P. (2023). A Synthetic ERR Agonist Alleviates Metabolic Syndrome. Journal of Pharmacology and Experimental Therapeutics, 387(2), 350-362. PubMed
   
8. Alexopoulos, S.J., Chen, S.Y., Brandon, A.E., Salamoun, J.M., Byrne, F.L., Garcia, C.J., Hoehn, K.L. (2020). Mitochondrial uncoupler BAM15 reverses diet-induced obesity and insulin resistance in mice. Nature Communications, 11(1), 2397. PubMed
   
9. Axelrod, C.L., King, W.T., Davuluri, G., Noland, R.C., Hall, J., Hull, M., Dantas, W.S., Zunica, E.R., Alexopoulos, S.J., Hoehn, K.L., & Kirwan, J.P. (2020). BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control. EMBO Molecular Medicine, 12(7), e12088. PubMed
   
10. Shahien, A., Bowman, J.D., Verschueren, E., Collins, M., Zhu, S., Xiao, J., Li, G., Svensson, S., Arao, Y., Huang, P., Yulyaningsih, E., Tombler, E., Wu, Y., Shapira, S.N., Xu, H.E., Kojetin, D.J., Seale, P., Weiss, J.M., & Burris, T.P. (2020). Modulation of estrogen-related receptors subtype selectivity: Conversion of an ERRβ/γ selective agonist to ERRα/β/γ pan agonists. Bioorganic Chemistry, 102, 104079. PubMed
    
11. Dierickx, P., Saad, N.S., Boone, C.H., Toh, J.D., Billon, C., Chen, J., Garcia, E., Anderson, P.E., Perez-Ramirez, C.A., Plotkin, D.L., Emmett, M.J., & Burris, T.P. (2023). Abstract 9682: The Cardiac Protective Effects of Novel Synthetic Pan-Estrogen Related Receptor Agonists Slu-pp-332 and Slu-pp-915. Circulation, 148(Suppl_1), A9682.
12. Konze, S.A., van Diepen, J.A., Schröder, J., Oliverio, M., Rensen, P.C., Keijer, J., & Lombès, M. (2023). BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils. Journal of Clinical Investigation, 133(7), e152401. PubMed
    
13. Xiong, G., Zhang, K., Ma, Y., Song, Y., Zhang, W., Qi, T., Qiu, H., Shi, J., Kan, C., Zhang, J., & Sun, X. (2023). BAM15 as a mitochondrial uncoupler: a promising therapeutic agent for diverse diseases. Frontiers in Endocrinology, 14, 1252141. PubMed
    
14. Berrougui, H., Herkat, B., Khalil, A., & Fulop, T. (2021). Breast cancer growth and proliferation is suppressed by the mitochondrial targeted furazano[3,4-b]pyrazine BAM15. Cancer & Metabolism, 9(1), 37. PubMed
    
15. Wang, Z., Ying, Z., Bosy-Westphal, A., Zhang, J., Schautz, B., Later, W., Heymsfield, S.B., & Müller, M.J. (2011). Specific metabolic rates of major organs and tissues across adulthood: evaluation by mechanistic model of resting energy expenditure. American Journal of Clinical Nutrition, 92(6), 1369-1377. (Note: Cited for allometric scaling principles)

All references open in new window. These citations are provided for educational and research purposes only. This information is not intended to diagnose, treat, cure, or prevent any disease. SLU-PP-332+BAM15 is intended for laboratory research use only.