SS 31

SS-31 (Elamipretide) Research Peptide – Mitochondrial Function, Cardiolipin & Cellular Energy Research

Mitochondria-Targeting Tetrapeptide for Cardiolipin Biology, Oxidative Phosphorylation, ATP Production, Oxidative Stress & Mitochondrial Disease Research

SS-31, also known as Elamipretide, MTP-131 and Bendavia, is a synthetic mitochondria-targeting tetrapeptide investigated for its interaction with cardiolipin, a specialized phospholipid concentrated in the inner mitochondrial membrane.

SS-31 belongs to the Szeto–Schiller family of aromatic-cationic peptides. Its structure allows it to interact with mitochondrial membrane components involved in cellular energy production.

Unlike conventional peptide hormones, SS-31 is not primarily studied as an endocrine receptor agonist. Its research focuses on mitochondrial membrane organization, respiratory chain function and cellular responses to mitochondrial stress.

SS-31 has been investigated in laboratory experiments, animal models and human clinical trials.

Its principal research areas include:

• Mitochondrial membrane biology

• Cardiolipin binding and organization

• Mitochondrial cristae structure

• Electron transport chain function

• Oxidative phosphorylation

• Adenosine triphosphate (ATP) production

• Reactive oxygen species (ROS) regulation

• Cytochrome c interactions

• Mitochondrial dysfunction

• Skeletal muscle bioenergetics

• Cardiac mitochondrial research

• Renal mitochondrial injury models

• Neuronal mitochondrial research

• Ischemia–reperfusion injury

• Cellular aging and mitochondrial stress

• Mitochondrial peptide pharmacology

Important regulatory update: On September 19, 2025, the US Food and Drug Administration granted accelerated approval to Forzinity (elamipretide) for improving muscle strength in adults and children with Barth syndrome weighing at least 30 kg.

This authorization applies to the specific approved pharmaceutical product and indication. It does not establish SS-31 as a general anti-aging, performance-enhancing or mitochondrial optimization treatment.

ICAME Pharmacy SS-31 is intended exclusively for laboratory research and development purposes.

FOR RESEARCH USE ONLY — NOT FOR HUMAN OR VETERINARY USE.

What Is SS-31?

SS-31 is a synthetic four-amino-acid peptide developed to investigate mitochondrial function.

Its amino acid sequence is:

D-Arg–2,6-dimethyl-Tyr–Lys–Phe–NH₂

The molecule contains:

• D-arginine

• 2,6-dimethyl-L-tyrosine

• L-lysine

• L-phenylalaninamide

The combination of positively charged and aromatic amino acid residues contributes to its interaction with biological membranes.

SS-31 is associated with research into mitochondrial cardiolipin, electron transport and cellular energy metabolism.

The compound has attracted scientific interest because mitochondrial dysfunction is involved in numerous biological processes, including inherited mitochondrial disorders, tissue injury and age-associated cellular changes.

However, the presence of mitochondrial dysfunction in a disease does not establish that SS-31 can successfully treat that disease.

SS-31 Molecular Structure and Chemical Properties

SS-31 is a linear tetrapeptide containing four amino acid residues.

Its structure includes an unusual modified tyrosine residue and a C-terminal amide.

Molecular Characteristics

The molecular formula and weight describe the elamipretide molecular entity, not every possible salt or formulation.

For example, the approved Forzinity formulation contains elamipretide hydrochloride, which has a different total molecular composition from the free peptide.

SS-31 Amino Acid Sequence

The full peptide sequence is:

H-D-Arg–Dmt–Lys–Phe–NH₂

Here, Dmt represents 2,6-dimethyltyrosine.

The alternating aromatic and cationic characteristics are important to SS-31's membrane-associated pharmacology.

Why Is the D-Arginine Residue Important?

D-amino acids have stereochemistry different from naturally occurring L-amino acids.

Incorporating D-arginine can influence peptide interactions and enzymatic susceptibility.

The D-arginine residue is an intentional structural feature of SS-31.

Why Is Dimethyltyrosine Important?

The modified tyrosine residue contributes aromatic characteristics to the molecule.

Its structural properties influence the peptide's physicochemical behavior.

SS-31 should not be treated as equivalent to an unmodified arginine–tyrosine–lysine–phenylalanine peptide.

What Are Mitochondria?

Mitochondria are cellular organelles involved in energy metabolism and numerous signaling processes.

They participate in the conversion of nutrients into usable cellular energy.

One of their central functions is the production of ATP through oxidative phosphorylation.

Mitochondria also contribute to:

Calcium regulation

Reactive oxygen species signaling

Cellular metabolism

Apoptosis-associated pathways

Stress responses

Metabolic adaptation

Cellular homeostasis

Mitochondrial function depends on coordinated interactions among proteins, lipids and metabolic substrates.

Understanding Mitochondrial Structure

A mitochondrion contains several major compartments.

Outer Mitochondrial Membrane

The outer membrane separates the organelle from the surrounding cytoplasm.

Intermembrane Space

This region participates in the proton gradient used for ATP production.

Inner Mitochondrial Membrane

The inner membrane contains the major protein complexes involved in oxidative phosphorylation.

Cristae

Cristae are folds of the inner mitochondrial membrane.

They increase membrane surface area and contribute to the spatial organization of respiratory proteins.

Mitochondrial Matrix

The matrix contains enzymes involved in metabolic processes, mitochondrial DNA and other molecular components.

SS-31 research focuses particularly on the inner mitochondrial membrane and cardiolipin-associated organization.

What Is Cardiolipin?

Cardiolipin is a specialized phospholipid enriched in the inner mitochondrial membrane.

It has a distinctive structure containing four fatty acyl chains.

Cardiolipin contributes to several mitochondrial functions.

Major Biological Roles

Respiratory chain organization

Membrane curvature

Cristae structure

Protein–lipid interactions

Electron transport chain stability

Cytochrome c interactions

Mitochondrial stress responses

Cardiolipin composition and remodeling are important for normal mitochondrial physiology.

Disruption of cardiolipin metabolism is particularly relevant to Barth syndrome.

How Does SS-31 Work?

SS-31 interacts with cardiolipin in the inner mitochondrial membrane.

Experimental evidence indicates that electrostatic and hydrophobic interactions contribute to this association.

By interacting with cardiolipin, SS-31 may influence mitochondrial membrane organization and protein–lipid interactions.

Its biological effects have been investigated in relation to mitochondrial respiration, reactive oxygen species and cellular stress.

Proposed Mechanism of Action

SS-31 (Elamipretide)

↓

Cellular Uptake and Mitochondrial Localization

↓

Interaction With Inner-Membrane Cardiolipin

↓

Changes in Cardiolipin-Associated Membrane Organization

↓

Potential Effects on Respiratory Chain Function

↓

Changes in Mitochondrial Bioenergetics and Stress Responses

↓

Measured Cellular or Tissue Outcomes

The strength and direction of these effects depend on the experimental system.

SS-31 should not be described as universally increasing ATP production in every cell or tissue.

SS-31 and the Inner Mitochondrial Membrane

The inner mitochondrial membrane contains protein complexes involved in oxidative phosphorylation.

Its lipid composition is essential for normal function.

Cardiolipin helps organize respiratory chain proteins and maintain mitochondrial membrane architecture.

SS-31 has been investigated for its ability to interact with this membrane environment.

Research Areas

Cardiolipin binding

Membrane structure

Cristae organization

Protein–lipid interactions

Mitochondrial respiration

Membrane-associated signaling

Bioenergetic responses

These interactions provide a mechanistic foundation for investigating SS-31 in mitochondrial disease models.

SS-31 and the Electron Transport Chain

The mitochondrial electron transport chain contains several protein complexes.

These complexes transfer electrons and contribute to formation of the proton gradient used for ATP synthesis.

Principal Components

Complex I — NADH Oxidoreductase

Complex II — Succinate Dehydrogenase

Complex III — Cytochrome bc₁ Complex

Complex IV — Cytochrome c Oxidase

Complex V — ATP Synthase

Cardiolipin supports the structural and functional organization of several respiratory chain components.

SS-31 has been investigated for its effects on cardiolipin-associated respiratory function.

Important Distinction

SS-31 is not an electron transport chain complex.

It does not directly replace respiratory proteins or mitochondrial enzymes.

Its proposed effects arise from interactions with the mitochondrial membrane environment.

SS-31 and Oxidative Phosphorylation

Oxidative phosphorylation is a major process by which mitochondria produce ATP.

It depends on coordinated electron transport and proton-gradient utilization.

Mitochondrial dysfunction can reduce the efficiency of this process.

SS-31 has been studied in models of impaired mitochondrial respiration.

Experimental Endpoints

Oxygen consumption rate

ATP-linked respiration

Maximal respiratory capacity

Respiratory coupling efficiency

Mitochondrial membrane potential

Electron transport efficiency

Reactive oxygen species generation

However, improved respiration in a laboratory model does not automatically establish improved exercise performance or health outcomes in humans.

SS-31 and ATP Production

Adenosine triphosphate is a major energy-carrying molecule used by cells.

Mitochondria produce ATP through oxidative phosphorylation.

Because SS-31 interacts with cardiolipin-associated mitochondrial structures, researchers have investigated its effects on ATP production.

Research Questions

Can cardiolipin-associated membrane changes affect ATP synthesis?

Does SS-31 alter oxygen consumption in stressed cells?

Are ATP-associated changes dependent on mitochondrial disease mechanisms?

Do observed effects vary between tissues?

Are changes sustained over time?

Preclinical studies have reported favorable bioenergetic effects in selected models.

These findings should not be generalized to all human populations.

SS-31 and Reactive Oxygen Species

Reactive oxygen species are produced during normal cellular metabolism.

At controlled levels, ROS participate in cellular signaling.

Excessive ROS generation can contribute to oxidative damage.

Mitochondrial dysfunction may alter ROS production and handling.

SS-31 has been investigated in experimental models involving oxidative stress.

Research Areas

Mitochondrial ROS

Oxidative damage markers

Respiratory chain-associated electron leakage

Lipid oxidation

Cellular antioxidant responses

Stress-associated signaling

Mitochondrial membrane integrity

SS-31 should not be described as eliminating ROS or acting as a universal antioxidant.

ROS have both physiological and pathological roles.

SS-31 and Cytochrome c Research

Cytochrome c is a mitochondrial protein involved in electron transfer between respiratory complexes.

It also participates in apoptosis-associated signaling.

Cardiolipin interacts with cytochrome c in the inner mitochondrial membrane.

Under certain conditions, changes in cardiolipin–cytochrome c interactions are associated with lipid oxidation and cellular stress responses.

SS-31 has been investigated for its influence on these interactions.

Research Topics

Cytochrome c–cardiolipin binding

Cardiolipin oxidation

Mitochondrial membrane integrity

Electron transfer

Apoptosis-associated pathways

Cellular injury responses

However, these findings do not establish that SS-31 universally prevents apoptosis or cell death.

SS-31 and Mitochondrial Cristae Research

Cristae are folds of the inner mitochondrial membrane.

Their architecture is important for efficient mitochondrial organization.

Cardiolipin contributes to membrane curvature and structural stability.

SS-31 has been investigated in models involving altered cristae morphology.

Research Areas

Cristae organization

Mitochondrial ultrastructure

Membrane curvature

Electron microscopy

Respiratory chain organization

Mitochondrial stress

Some studies have reported improvements in mitochondrial morphology under experimental conditions.

However, structural changes do not necessarily translate into clinical benefit.

SS-31 and Barth Syndrome Research

Barth syndrome is a rare inherited disorder associated with mitochondrial cardiolipin metabolism.

It is caused by pathogenic variants in the TAZ gene, which encodes tafazzin.

Tafazzin participates in cardiolipin remodeling.

Abnormal cardiolipin composition contributes to mitochondrial dysfunction.

Barth syndrome can involve:

Skeletal muscle weakness

Cardiomyopathy

Exercise intolerance

Neutropenia

Growth abnormalities

Mitochondrial bioenergetic dysfunction

Because SS-31 interacts with cardiolipin, it became a candidate for investigation in Barth syndrome.

SS-31 and the TAZ Gene

The TAZ gene encodes tafazzin, an enzyme involved in cardiolipin remodeling.

TAZ-associated dysfunction alters cardiolipin composition.

This can affect mitochondrial structure and function.

Research Areas

Cardiolipin remodeling

Monolysocardiolipin accumulation

Respiratory chain organization

Mitochondrial morphology

Skeletal muscle function

Cardiac mitochondrial biology

SS-31 does not replace the TAZ gene or correct the underlying genetic variant.

Its pharmacological approach involves interaction with mitochondrial cardiolipin.

SS-31 Clinical Research in Barth Syndrome

Elamipretide has been evaluated in a small clinical development program involving patients with Barth syndrome.

The program included randomized controlled research and longer-term extension observations.

TAZPOWER Research

The TAZPOWER program investigated elamipretide in individuals with genetically confirmed Barth syndrome.

Researchers evaluated outcomes including:

Muscle strength

Six-minute walk distance

Fatigue-related symptoms

Patient-reported outcomes

Cardiac measurements

Safety and tolerability

The initial controlled study was small, and some endpoints did not demonstrate statistically significant differences during the randomized phase.

Long-term open-label observations reported improvements in selected outcomes.

However, open-label findings are more susceptible to bias than blinded controlled comparisons.

FDA Accelerated Approval of Elamipretide

On September 19, 2025, the FDA granted accelerated approval to Forzinity (elamipretide).

The approved indication is to improve muscle strength in adults and pediatric patients with Barth syndrome weighing at least 30 kg.

The accelerated approval was based on improvement in knee extensor muscle strength, an intermediate clinical endpoint.

What Accelerated Approval Means

Accelerated approval allows the FDA to authorize certain medicines for serious conditions based on an endpoint considered reasonably likely to predict clinical benefit.

Continued approval may depend on confirmatory research.

Important Limitations

The approval does not establish that elamipretide:

• Treats every mitochondrial disease

• Improves athletic performance

• Reverses biological aging

• Prevents neurodegenerative disease

• Treats all forms of muscle weakness

• Restores mitochondrial function in healthy individuals

• Provides generalized cardiovascular protection

The authorization applies to a specific pharmaceutical formulation and patient population.

Research-grade SS-31 is not an FDA-approved substitute for Forzinity.

SS-31 and Primary Mitochondrial Myopathy

Primary mitochondrial myopathies are inherited disorders affecting mitochondrial energy production.

They can cause muscle weakness, fatigue and exercise intolerance.

SS-31 has been investigated in clinical trials involving these conditions.

Research Endpoints

Six-minute walk distance

Fatigue scores

Muscle function

Patient-reported outcomes

Physical performance

Safety and tolerability

The results have not been uniformly positive.

MMPOWER-3 Phase 3 Clinical Trial

The MMPOWER-3 trial evaluated elamipretide in 218 participants with genetically confirmed primary mitochondrial myopathy.

Participants were randomized to elamipretide or placebo.

The study evaluated outcomes after 24 weeks.

Primary Endpoints

Six-minute walk test

Total fatigue score

Results

The trial did not meet its primary efficacy endpoints.

The difference between treatment groups in six-minute walk distance was not statistically significant.

The difference in total fatigue scores was also not statistically significant.

These results are important because they demonstrate that promising preclinical mitochondrial mechanisms do not guarantee successful clinical outcomes.

Scientific Interpretation

The negative MMPOWER-3 results do not invalidate every experimental finding involving SS-31.

However, they limit claims of broad clinical effectiveness in primary mitochondrial myopathy.

SS-31 and Skeletal Muscle Research

Skeletal muscle requires substantial ATP production during physical activity.

Mitochondrial dysfunction can affect muscle endurance and cellular energy metabolism.

SS-31 has been investigated in muscle-related research.

Research Areas

Mitochondrial respiration

Muscle energy metabolism

Exercise-associated mitochondrial stress

Oxidative phosphorylation

Muscle fatigue

Mitochondrial disease

Cardiolipin-associated function

The approved Barth syndrome indication concerns a specific rare disease.

It does not establish muscle-building benefits in healthy individuals.

SS-31 and Muscle Strength

Muscle strength depends on multiple biological systems.

These include muscle structure, neural activation, metabolism and mechanical loading.

Mitochondrial function is particularly important for sustained cellular energy production.

SS-31's clinical development has included muscle strength measurements.

However, findings in Barth syndrome cannot be generalized to bodybuilding, athletic performance or age-related muscle loss.

SS-31 and Exercise Endurance Research

Exercise endurance depends on cardiovascular, respiratory, muscular and metabolic systems.

Mitochondrial oxidative phosphorylation contributes to sustained activity.

SS-31 has been investigated in experimental and clinical settings involving exercise-related endpoints.

Research Areas

Mitochondrial oxygen consumption

Muscle bioenergetics

Exercise intolerance

Fatigue-associated measurements

Physical performance testing

Mitochondrial disease models

However, SS-31 is not an established endurance-enhancing treatment for healthy individuals.

SS-31 and Cardiac Mitochondrial Research

Cardiac muscle has high energy requirements.

Mitochondrial ATP production is essential for normal cardiac function.

Cardiolipin contributes to respiratory chain organization in cardiac mitochondria.

SS-31 has been investigated in experimental cardiac models.

Research Areas

Cardiac mitochondrial respiration

Ischemia–reperfusion injury

Cardiolipin-associated function

Mitochondrial oxidative stress

Cardiac energy metabolism

Mitochondrial membrane integrity

Some preclinical studies have reported favorable effects on cardiac mitochondrial endpoints.

However, SS-31 has not been established as a broadly effective treatment for heart failure or ischemic heart disease.

SS-31 and Ischemia–Reperfusion Injury

Ischemia occurs when tissue receives insufficient blood supply.

Reperfusion restores blood flow but can produce additional cellular stress.

Mitochondrial dysfunction and oxidative stress are involved in ischemia–reperfusion injury.

SS-31 has been investigated in experimental models of this process.

Research Areas

Mitochondrial ROS

Cellular energy depletion

Cardiolipin oxidation

Mitochondrial membrane damage

Inflammatory signaling

Tissue injury responses

However, experimental protection against ischemia–reperfusion injury does not establish clinical efficacy in humans.

SS-31 and Kidney Research

Kidney cells, particularly renal tubular cells, have substantial metabolic demands.

Mitochondrial function is important for renal transport processes.

SS-31 has been investigated in experimental models of kidney injury.

Research Areas

Renal mitochondrial respiration

Tubular epithelial cell stress

Oxidative injury

Ischemia–reperfusion models

Mitochondrial membrane integrity

Cellular recovery responses

Preclinical studies have reported changes in selected renal injury markers.

However, SS-31 is not an established treatment for chronic kidney disease or acute kidney injury.

SS-31 and Brain Research

Neurons depend on mitochondrial energy production.

Mitochondrial dysfunction can affect neuronal signaling and cellular survival.

SS-31 has been investigated in experimental neurological models.

Research Areas

Neuronal mitochondrial function

Oxidative stress

Mitochondrial membrane integrity

Neuroinflammatory signaling

Neuronal injury

Cellular bioenergetics

However, there is insufficient evidence establishing SS-31 as a clinically effective treatment for neurological disorders.

SS-31 and Neurodegenerative Disease Research

Mitochondrial dysfunction is associated with several neurodegenerative diseases.

These include Alzheimer's disease and Parkinson's disease.

SS-31 has been investigated in experimental systems relevant to neuronal mitochondrial dysfunction.

Research Areas

Mitochondrial respiration

Oxidative damage

Neuronal survival

Mitochondrial morphology

Neuroinflammatory pathways

Protein-associated cellular stress

However, SS-31 has not been established as a clinically effective treatment for Alzheimer's disease, Parkinson's disease or other neurodegenerative disorders.

SS-31 and Cellular Aging Research

Mitochondrial changes are associated with multiple aspects of biological aging.

These may include altered respiratory function, oxidative stress and mitochondrial quality-control processes.

SS-31 has been investigated in preclinical models involving age-associated mitochondrial dysfunction.

Research Areas

Age-associated mitochondrial respiration

Mitochondrial ROS

Skeletal muscle bioenergetics

Cellular stress responses

Mitochondrial ultrastructure

Tissue metabolism

Cardiolipin-associated changes

However, mitochondrial improvements in experimental systems do not establish reversal of human aging.

Does SS-31 Reverse Aging?

There is no established clinical evidence that SS-31 reverses biological aging or extends human lifespan.

Its effects on specific mitochondrial pathways should not be equated with comprehensive rejuvenation.

Claims involving longevity, anti-aging or biological age reduction remain unproven.

SS-31 and Mitochondrial Quality Control

Mitochondrial quality control involves several interconnected processes.

These include:

Mitochondrial dynamics

Mitophagy

Biogenesis

Protein quality control

Membrane maintenance

Cellular stress responses

SS-31 has been investigated in experimental systems measuring some of these processes.

However, it should not be described as a universal activator of mitochondrial biogenesis or mitophagy.

Its effects depend on the model and measured endpoint.

SS-31 and Mitochondrial Membrane Potential

The mitochondrial membrane potential is an electrochemical component of oxidative phosphorylation.

It reflects the movement and distribution of charged particles across the inner mitochondrial membrane.

Researchers use membrane-potential measurements to investigate mitochondrial function.

SS-31 has been studied in models involving altered membrane physiology.

Research Endpoints

Membrane potential

Mitochondrial respiration

ATP-linked activity

Cellular stress

Membrane integrity

Mitochondrial morphology

Membrane-potential changes require careful interpretation because both excessive and insufficient polarization can occur in pathological states.

SS-31 vs. MOTS-c

SS-31 and MOTS-c are distinct mitochondria-associated research peptides.

The two peptides have different structures and proposed mechanisms.

SS-31 vs. Humanin

Humanin is a mitochondria-derived peptide investigated in cellular stress and survival pathways.

SS-31 is a synthetic cardiolipin-interacting peptide.

The compounds should not be treated as functionally equivalent.

SS-31 vs. NAD+ Research

NAD+ is a metabolic cofactor involved in redox reactions and multiple cellular processes.

SS-31 is a peptide that interacts with mitochondrial cardiolipin.

SS-31

Research focus: Mitochondrial membrane structure and cardiolipin-associated bioenergetics.

NAD+

Research focus: Cellular redox metabolism, enzyme activity and metabolic signaling.

Although both are relevant to mitochondrial biology, their molecular identities and mechanisms differ.

SS-31 is not a replacement for NAD+.

SS-31 vs. Coenzyme Q10

Coenzyme Q10 is a lipid-soluble molecule involved in mitochondrial electron transport.

SS-31 is a synthetic peptide associated with cardiolipin.

Both are relevant to mitochondrial research, but their mechanisms are different.

SS-31 vs. BPC-157

BPC-157 is a synthetic 15-amino-acid peptide investigated primarily in preclinical tissue injury and gastrointestinal models.

SS-31 is a four-amino-acid mitochondria-targeting peptide.

Findings involving BPC-157 cannot establish the effects of SS-31.

SS-31 Clinical Evidence: What Has Been Established?

SS-31 has a more developed clinical research history than many experimental peptides.

However, the results differ across diseases.

Barth Syndrome

Elamipretide received FDA accelerated approval in 2025 for improving muscle strength in a defined Barth syndrome population.

Primary Mitochondrial Myopathy

The MMPOWER-3 phase 3 trial did not demonstrate statistically significant improvement in its primary walking-distance or fatigue endpoints.

Other Mitochondrial-Related Conditions

Investigations have been conducted in additional clinical and experimental settings.

However, broad efficacy across mitochondrial disorders has not been established.

Healthy Adults

Reliable evidence supporting anti-aging, bodybuilding, athletic performance or general energy-enhancement claims is insufficient.

SS-31 Safety Considerations

SS-31's safety profile depends on the specific formulation and clinical context.

The approved Forzinity product has undergone regulatory evaluation for its authorized indication.

However, research-grade SS-31 is not equivalent to the approved medicine.

Reported Adverse Reactions

Clinical studies and the approved product labeling identify injection-site reactions as common adverse events.

Hypersensitivity

Serious hypersensitivity to elamipretide or product ingredients is a contraindication for Forzinity.

Formulation-Related Risks

Safety depends on excipients, manufacturing controls and pharmaceutical quality.

Renal Function

The approved Forzinity labeling includes specific considerations for severe renal impairment.

Long-Term Safety

Long-term safety outside studied populations and approved indications remains incompletely characterized.

Unknown Benefits in Healthy Individuals

No established clinical benefit supports nonmedical SS-31 use for longevity or performance enhancement.

The safety findings of an approved pharmaceutical product cannot be assumed to apply to research-grade peptide preparations.

SS-31 Regulatory Status

United States

Forzinity (elamipretide) received FDA accelerated approval on September 19, 2025.

The approved indication is limited to improving muscle strength in adults and pediatric patients with Barth syndrome weighing at least 30 kg.

European Union

US FDA approval does not automatically provide marketing authorization in the European Union.

EU regulatory status must be evaluated separately for the specific pharmaceutical product.

Research Products

Research-grade SS-31 products are not automatically approved medicines.

The existence of an FDA-approved elamipretide formulation does not authorize other products for clinical use.

SS-31 Analytical Characterization

Accurate molecular identification is essential for peptide research.

SS-31 contains an unusual modified tyrosine residue and a D-amino acid.

These features require appropriate analytical verification.

Important Quality Parameters

Verified peptide sequence

Correct amino acid stereochemistry

Molecular identity

Molecular mass

C-terminal amidation

Peptide purity

Peptide content

Counterion composition

Residual reagents

Degradation products

Batch-specific analytical documentation

High-Performance Liquid Chromatography

HPLC can be used to evaluate SS-31 purity and chromatographic impurities.

However, chromatographic purity alone does not establish identity, correct stereochemistry or pharmaceutical suitability.

Liquid Chromatography–Mass Spectrometry

LC-MS can help verify the molecular mass of SS-31.

For the unmodified elamipretide molecular entity, the expected average molecular weight is approximately 639.8 g/mol.

Mass spectrometry should be interpreted in relation to the specified chemical form.

Stereochemical Identity

SS-31 contains D-arginine and other residues with defined stereochemistry.

Stereochemical identity matters because different configurations can influence biological activity.

A molecular mass measurement alone may not distinguish stereoisomers.

Appropriate identity testing may therefore require additional analytical methods.

Counterion and Salt Characterization

Elamipretide can be supplied in different salt forms.

For example, the approved Forzinity pharmaceutical product contains elamipretide hydrochloride.

A research preparation may have a different counterion composition.

The total mass of a salt form is not necessarily equal to the mass of the free peptide.

Batch-specific documentation should identify the actual chemical form.

Certificate of Analysis

A batch-specific Certificate of Analysis should contain relevant analytical information.

Recommended documentation includes:

• Product identity

• Batch or lot number

• Molecular formula

• Molecular mass

• Peptide sequence

• Stereochemical identity

• Peptide purity

• Peptide content

• Counterion information

• Analytical methodology

• Impurity profile

• Stability information

A COA does not establish clinical efficacy or authorization for human administration.

Scientific Evidence and Research Limitations

Established Scientific Facts

• SS-31 is a synthetic tetrapeptide.

• Elamipretide is its international nonproprietary name.

• Its sequence is D-Arg–2,6-dimethyl-Tyr–Lys–Phe–NH₂.

• Its molecular formula is C₃₂H₄₉N₉O₅.

• Its molecular weight is approximately 639.8 g/mol.

• Its principal molecular interaction involves mitochondrial cardiolipin.

• It has been studied in laboratory and animal mitochondrial dysfunction models.

• Human clinical trials have been conducted.

• The MMPOWER-3 trial did not meet its primary efficacy endpoints.

• Forzinity received FDA accelerated approval for a specific Barth syndrome indication in September 2025.

Important Limitations

• SS-31 is not established as a universal mitochondrial enhancer.

• It does not replace defective mitochondrial genes.

• Clinical efficacy differs across disease populations.

• Anti-aging benefits are unproven.

• Human lifespan extension has not been established.

• General muscle-building effects are unproven.

• Athletic performance enhancement is not established.

• Neurodegenerative disease treatment benefits remain unproven.

• The FDA approval applies to Forzinity, not every elamipretide preparation.

• Research-grade SS-31 is not an approved pharmaceutical substitute.

Potential SS-31 Research Applications

SS-31 may be relevant to appropriately controlled laboratory investigations involving:

• Mitochondrial cardiolipin

• Inner mitochondrial membrane structure

• Mitochondrial cristae

• Respiratory chain organization

• Oxidative phosphorylation

• ATP production

• Oxygen consumption

• Reactive oxygen species

• Cytochrome c interactions

• Cardiolipin oxidation

• Mitochondrial stress responses

• Barth syndrome biology

• TAZ-associated cardiolipin remodeling

• Primary mitochondrial myopathy

• Skeletal muscle bioenergetics

• Cardiac mitochondrial function

• Renal mitochondrial research

• Neuronal mitochondrial research

• Ischemia–reperfusion injury

• Cellular aging models

• Mitochondrial ultrastructure

• Peptide structure–activity relationships

• Analytical peptide characterization

These are scientific research applications. They do not establish therapeutic benefits for ICAME Pharmacy research products.

SS-31 Research Overview

Compound Name: SS-31

International Nonproprietary Name: Elamipretide

Alternative Names: MTP-131 / Bendavia

Classification: Synthetic Mitochondria-Targeting Tetrapeptide

Peptide Length: 4 Amino Acids

Sequence: D-Arg–2,6-dimethyl-Tyr–Lys–Phe–NH₂

Molecular Formula: C₃₂H₄₉N₉O₅

Molecular Weight: Approximately 639.8 g/mol

CAS Number: 736992-21-5

PubChem CID: 11764719

Primary Molecular Interaction: Cardiolipin

Principal Research Location: Inner Mitochondrial Membrane

Research Areas: Mitochondrial Function / ATP Production / Oxidative Stress / Cardiolipin Biology

FDA Status: Forzinity received accelerated approval in September 2025 for a defined Barth syndrome indication.

ICAME Product Status: Research Use Only

ICAME Pharmacy Product Information

Product Name: SS-31

Alternative Names: Elamipretide / MTP-131 / Bendavia

Brand: ICAME Pharmacy

Product Category: Research Peptide

Research Classification: Mitochondria-Targeting Aromatic-Cationic Tetrapeptide

Research Areas: Mitochondrial Biology / Cardiolipin / Oxidative Phosphorylation / Cellular Bioenergetics

Intended Use: Laboratory Research & Development Only

Product identity and specifications should be verified using batch-specific analytical documentation.

Relevant quality information includes:

• Verified peptide sequence

• Molecular identity

• Stereochemical identity

• Peptide purity

• Peptide content

• Counterion composition

• Impurity profile

• Analytical methodology

• Certificate of Analysis (COA)

• Batch or lot identification

• Validated stability and storage conditions

No claims of pharmaceutical quality, sterility, injectable suitability or clinical equivalence to Forzinity should be made without appropriate authorization and supporting documentation.

Important Research Use Notice

FOR RESEARCH USE ONLY (RUO)

This ICAME Pharmacy product is intended exclusively for legitimate laboratory, analytical and scientific research purposes.

Not for human or veterinary use. Not for diagnostic, therapeutic, anti-aging, longevity, bodybuilding, athletic performance enhancement or other clinical purposes. Not for direct administration to humans or animals.

SS-31, also known as elamipretide, is a synthetic tetrapeptide investigated in mitochondrial biology and clinical research.

The FDA granted accelerated approval to the specific pharmaceutical product Forzinity in September 2025 for improving muscle strength in a defined Barth syndrome population.

ICAME Pharmacy SS-31 is not Forzinity and is not an FDA-approved medicine.

The approved indication for Forzinity does not establish the safety, efficacy or suitability of research-grade SS-31 for human administration.

Information presented on this page is intended solely for scientific and educational purposes and does not constitute medical advice, prescribing information, dosage guidance or instructions for human use.

About ICAME Pharmacy

ICAME Pharmacy provides specialized research products for professional laboratory and scientific applications.

Our portfolio focuses on compounds relevant to peptide science, mitochondrial biology, molecular signaling, cellular bioenergetics and analytical chemistry.

We emphasize accurate product identification, responsible research use, scientific transparency and clear communication of evidence limitations.

For batch-specific analytical documentation and product inquiries, please contact ICAME Pharmacy.

Frequently Asked Questions About SS-31

What is SS-31?

SS-31 is a synthetic four-amino-acid peptide investigated for its interactions with mitochondrial cardiolipin.

What is another name for SS-31?

Elamipretide is its international nonproprietary name. MTP-131 and Bendavia are additional names.

How many amino acids does SS-31 contain?

Four amino acids.

What is the amino acid sequence of SS-31?

D-Arg–2,6-dimethyl-Tyr–Lys–Phe–NH₂.

What is the molecular formula of SS-31?

C₃₂H₄₉N₉O₅.

What is the molecular weight of SS-31?

Approximately 639.8 g/mol for the elamipretide molecular entity.

What is the CAS number of SS-31?

736992-21-5.

What is the primary molecular target of SS-31?

SS-31 interacts with cardiolipin in the inner mitochondrial membrane.

What is cardiolipin?

Cardiolipin is a specialized phospholipid involved in mitochondrial membrane structure and respiratory chain organization.

How does SS-31 work?

SS-31 interacts with mitochondrial cardiolipin and has been investigated for effects on membrane organization, respiration and cellular stress responses.

Does SS-31 increase ATP production?

Some experimental models have reported favorable effects on mitochondrial bioenergetics. However, universal ATP enhancement in humans has not been established.

Does SS-31 reduce oxidative stress?

Some preclinical studies reported changes in oxidative stress markers. The effects depend on the experimental model.

Is SS-31 an antioxidant?

SS-31 is primarily characterized as a mitochondria-targeting cardiolipin-interacting peptide, not as a conventional universal antioxidant.

Is SS-31 FDA-approved?

A specific elamipretide pharmaceutical product, Forzinity, received FDA accelerated approval in September 2025 for a defined Barth syndrome indication.

What is Forzinity?

Forzinity is an FDA-approved elamipretide pharmaceutical product indicated to improve muscle strength in adults and children with Barth syndrome weighing at least 30 kg.

Is research-grade SS-31 the same as Forzinity?

No. Research-grade SS-31 is not equivalent to the approved pharmaceutical formulation.

Has SS-31 been studied in humans?

Yes. Elamipretide has been evaluated in multiple clinical studies.

What happened in the MMPOWER-3 trial?

The phase 3 trial did not demonstrate statistically significant improvement in its primary walking-distance or fatigue endpoints.

Does SS-31 treat every mitochondrial disease?

No. Clinical efficacy has not been established across all mitochondrial diseases.

Does SS-31 improve muscle strength?

Forzinity has a specific FDA-approved indication involving muscle strength in Barth syndrome. This does not establish general muscle-strength benefits in healthy people.

Does SS-31 build muscle?

Reliable clinical evidence supporting bodybuilding benefits is lacking.

Does SS-31 improve athletic endurance?

SS-31 has not been established as an effective endurance-enhancing treatment for healthy individuals.

Does SS-31 reverse aging?

No. Human anti-aging or lifespan-extension benefits have not been established.

Does SS-31 treat Alzheimer's disease?

No clinically established treatment benefit has been demonstrated.

Is SS-31 the same as MOTS-c?

No. SS-31 is a synthetic tetrapeptide, while MOTS-c is a mitochondria-derived peptide with a different structure and research mechanism.

Is SS-31 the same as Humanin?

No. Humanin and SS-31 are structurally distinct peptides.

Is SS-31 safe for human use?

The approved Forzinity product has a defined regulatory safety profile for its authorized indication. Research-grade SS-31 has not been established as suitable for human administration.

Is ICAME Pharmacy SS-31 intended for human use?

No. ICAME Pharmacy SS-31 is intended strictly for laboratory research and development purposes.