Twelve peptide monographs, one clinician network, and a monitoring loop that treats every regimen as a measured experiment on you — not a guess. Sequencing and bloodwork first; a licensed prescriber second; a compounded vial and a re-test date third.
Binary Helix does not prescribe. HelixCare Clinics — our partner telehealth and clinic network — holds the prescriptive authority, reviews your MyHelix data, and owns every dosing decision. We supply the sequencing, the informatics, the vials and the re-test cadence.
01
MyHelix profile & baseline bloodwork
You start inside MyHelix: whole-genome or targeted panel, medication and supplement history, symptoms, goals, and a baseline blood draw (metabolic, inflammatory, hormonal and — for mitochondrial work — the Binary Helix mRNA panel). Your data stays in your wallet; you grant the clinician time-boxed read access.
A licensed HelixCare prescriber reviews the file, screens eligibility and contraindications (cancer history, pregnancy or lactation, renal and hepatic function, interacting medications), and decides whether a peptide regimen is appropriate at all. Many consults end with lifestyle, nutrient or referral recommendations and no prescription — that is a legitimate outcome.
03
Personalised regimen, compounded and shipped
Where legally permitted, the prescription is dispensed through licensed 503A and 503B compounding pharmacy partners and shipped cold-chain in Binary Helix vials with reconstitution instructions, a dosing card, sterile supplies and a sharps return envelope. Availability of any given peptide varies by jurisdiction and by the pharmacy's own bulk-substance permissions.
Every regimen ships with a re-test date. MyHelix prompts symptom check-ins, flags adverse events for clinician review, and schedules biomarker re-draws at the interval set for your protocol. The prescriber adjusts dose, frequency, cycle length — or stops the regimen. No protocol is open-ended.
Prescription-only, gate-kept
Nothing in this library can be added to a cart. Rx items are dispensed only after HelixCare clinician approval in eligible jurisdictions.
Investigational by default
Most peptides here are not FDA-approved for the uses discussed. Where an approval exists, we name the exact indication rather than implying a general one.
Measured, not promised
Each monograph lists the labs we watch and the evidence grade behind it. Where the evidence is preclinical, we say so in the badge.
The library
Twelve molecules. Twelve monographs.
Open any monograph: mechanism, the protocol framework clinicians report using, the labs we monitor, the cautions, and an honest evidence grade.
Every dose range below is an illustrative clinician protocol framework — a summary of what practitioners report using, or of an approved label where one exists. Final dosing, eligibility and monitoring are determined by a licensed HelixCare Clinics prescriber.
Preclinical-dominantRx · Compounded
Pentadecapeptide BPC 157 · 15 amino acids · partial sequence of human gastric juice protein BPC.
BPC-157
Recovery & repair · Gastrointestinal
A stable 15-amino-acid peptide studied almost entirely in animal models of tendon, ligament, muscle, bone and gastrointestinal injury. Reported effects centre on angiogenesis and growth-factor signalling: in tendon explants and cultured tenocytes, BPC 157 promoted outgrowth, cell survival and migration11, and reviews of the preclinical programme frame it as acting through the same angiogenic growth-factor pathways that drive normal healing10.
Controlled human efficacy data are essentially absent. In the United States, the FDA has placed BPC-157 in the category of bulk drug substances that raise significant safety concerns for compounding, so legitimate pharmacy availability is restricted and varies by jurisdiction; where it is dispensed at all, it is dispensed as an investigational, non-approved substance.
Route
Subcutaneous injection, commonly near (not into) the target region; oral capsules or liquid are used specifically for gastrointestinal indications, where systemic absorption is limited.
Dose framework
250–500 mcg subcutaneously, once or twice daily — the range most often reported in clinical practice.
Frequency & cycle
Daily dosing for 4–8 weeks, then reassess. Practitioners typically stop at the end of a cycle rather than continue indefinitely.
Timing
Often split morning and evening; no established food interaction for the injectable form.
Storage & reconstitution
Lyophilised powder refrigerated; reconstitute with bacteriostatic water down the vial wall, swirl — never shake. Refrigerate after reconstitution, protect from light, and observe the pharmacy's beyond-use date (commonly 28–30 days).
Stacking notes
Paired with TB-500 as the widely discussed "Wolverine" repair stack — complementary rather than additive on paper: BPC-157 is framed as locally angiogenic, TB-500 as an actin-binding, cell-migration peptide. The combination has no controlled human trial behind it.
Sometimes run alongside a structured loading protocol (physiotherapy, progressive tendon loading). Loading has real evidence; the peptide does not. Clinicians should not let the peptide displace it.
Stacking with GH secretagogues compounds the growth-signalling caution below.
Monitoring & cautions
Monitor: CBC, CMP (renal and hepatic), hs-CRP, fasting glucose; blood pressure; injection-site inspection at every check-in; symptom-based functional measures for the injured tissue.
Caution — angiogenic mechanism: avoid in active malignancy and use only after explicit risk discussion in anyone with a cancer history. Pro-angiogenic and growth-promoting signalling is the same biology tumours exploit.
Not for use in pregnancy or lactation. Not studied in children.
Prohibited in sanctioned sport — BPC-157 is covered by the WADA Prohibited List; athletes should verify the current list before any use.
Preclinical-dominantRx · Compounded
Synthetic fragment of thymosin β4 containing the actin-binding domain.
TB-500
Thymosin β4 fragment · Repair
TB-500 is a short synthetic fragment of thymosin β4, a naturally occurring actin-sequestering peptide. The parent molecule has a genuinely broad regenerative literature — cell migration, angiogenesis, anti-inflammatory and anti-fibrotic effects across cornea, skin, heart and nervous tissue in animal models, with early clinical work in dry eye and wound healing1213.
Two honest caveats: nearly all of that evidence concerns full-length thymosin β4, not the TB-500 fragment sold for injection; and human efficacy data for musculoskeletal recovery are lacking. Evidence strength here is mechanistically rich, clinically thin.
Route
Subcutaneous injection (systemic intent — TB-500 is generally dosed for distribution rather than local effect).
Dose framework
Loading: ~2–2.5 mg SC twice weekly for 4–6 weeks. Maintenance: ~2 mg weekly or every other week, as reported in practice.
Frequency & cycle
Loading block, then maintenance or a full stop; cycles commonly capped at 8–12 weeks total before a washout and reassessment.
Timing
Time of day is not established as meaningful; consistency of interval matters more than clock time.
Storage & reconstitution
Lyophilised, refrigerated. Reconstitute with bacteriostatic water; do not shake. Refrigerate, use within the pharmacy's beyond-use date, and discard if cloudy or particulate.
Stacking notes
The other half of the "Wolverine" stack with BPC-157. Where clinicians run both, a common framework is BPC-157 daily plus TB-500 twice weekly through a 4–6 week loading block, then taper one at a time so any adverse effect can be attributed.
Avoid layering a third growth-promoting agent (GH secretagogues, IGF-1 analogues) on top — the risk profile stacks faster than the benefit.
GHK-Cu topical is sometimes added for dermal or scar-remodelling goals, where the tissue target is skin rather than tendon.
Monitoring & cautions
Monitor: CBC, CMP, hs-CRP, fasting glucose; injection-site review; objective function (range of motion, strength, return-to-activity milestones) rather than symptom impression alone.
Caution — angiogenic and pro-migratory mechanism: contraindicated in active malignancy; a cancer history warrants a documented risk conversation and often a decision not to prescribe.
Not for use in pregnancy or lactation; not studied in children.
Prohibited in sanctioned sport (thymosin β4 and its fragments fall under the WADA Prohibited List).
Limited human dataRx · Compounded
GHRH analogue paired with a selective ghrelin-receptor agonist.
CJC-1295 / Ipamorelin
GH axis · Recovery & body composition
A two-part growth-hormone secretagogue framework: a GHRH analogue (CJC-1295, with or without the drug-affinity-complex modification) combined with ipamorelin, a selective ghrelin-receptor agonist. Both act on the pituitary to increase endogenous GH pulsatility rather than replacing GH directly. Human pharmacology for GH secretagogues as a class is reasonably well characterised; controlled evidence for the specific anti-ageing, recovery and body-composition claims made in wellness practice is not.
Route
Subcutaneous injection, typically evening or bedtime to align with nocturnal GH pulsatility.
Dose framework
Reported practice ranges cluster around low-microgram-per-kilogram dosing of each component, most often 5 nights per week with 2 nights off, in cycles of 8–12 weeks. Ranges vary widely between clinics and are not label-derived — the prescriber sets them.
Monitoring
IGF-1 (the key titration marker), fasting glucose and HbA1c or an OGTT where risk exists, fasting insulin, thyroid panel, blood pressure; symptom review for oedema, arthralgia and carpal-tunnel-type symptoms.
Cautions
Contraindicated in active malignancy; caution with any cancer history, diabetes or impaired glucose tolerance (GH is counter-regulatory to insulin), untreated retinopathy, and pregnancy or lactation. Prohibited in sanctioned sport.
A naturally occurring copper-binding tripeptide present in human plasma, whose levels fall markedly with age. Gene-expression work reports that GHK-Cu modulates a large number of human genes in a direction associated with tissue remodelling — up-regulating collagen and antioxidant programmes while down-regulating inflammatory and fibrotic ones — and reviews summarise regenerative and protective actions across skin models1415.
The strongest practical evidence is topical and dermatological. Injectable GHK-Cu is not an approved drug and rests on extrapolation from cell, animal and topical studies. Copper is a bioactive metal, not an inert carrier — dose discipline matters.
Route
Topical serum or cream (best supported), or subcutaneous injection under prescription (investigational).
Dose framework — topical
1–3% GHK-Cu serum, once or twice daily to clean skin. Introduce on alternate days if the skin is reactive.
Dose framework — injectable
1–2 mg SC daily, 5 days per week, in 4–8 week cycles, as reported in clinical practice; washout between cycles.
Timing
Topical: avoid simultaneous application with strong direct acids, high-strength vitamin C or benzoyl peroxide — separate by time of day. Injectable: morning dosing is conventional, not evidence-based.
Storage & reconstitution
Powder refrigerated and protected from light; reconstituted solution has a characteristic blue tint from the copper complex. Refrigerate; discard on the beyond-use date or if colour or clarity changes.
Stacking notes
Topical + injectable is the common dual-route framework: the serum for photoaged facial skin, the injection for systemic or scar-remodelling intent. Count total copper exposure across both routes when dosing.
Pairs logically with collagen-supporting basics that do have evidence — retinoid at a separate time of day, daily broad-spectrum SPF, adequate protein and vitamin C intake.
Sometimes combined with TB-500 for scar or wound remodelling; no controlled data support the combination.
Monitoring & cautions
Monitor (injectable): serum copper and ceruloplasmin, CBC (copper–zinc interplay affects haematopoiesis), CMP with liver enzymes, zinc; photo-documented skin assessment for topical goals.
Contraindicated in Wilson disease and in any disorder of copper handling; caution in hepatic impairment.
Avoid in active malignancy — copper participates in angiogenesis.
Topical: patch-test for contact dermatitis; avoid application to broken skin unless directed. Not for use in pregnancy or lactation without prescriber sign-off.
Very limited dataRx · Compounded
Synthetic tetrapeptide Ala-Glu-Asp-Gly (AEDG).
Epitalon
Longevity · Pineal peptide analogue
A synthetic tetrapeptide derived from work on pineal extracts, promoted for circadian, telomere and longevity effects. We list it for completeness and grade it honestly: the published human literature is small, largely from a single research tradition, methodologically limited and not independently replicated. We do not present telomere-lengthening or lifespan claims as established.
Route
Subcutaneous or intramuscular injection; intranasal preparations also exist.
Dose framework
Reported practice uses short courses — on the order of 5–10 mg per dose given daily or on alternate days for 10–20 days, once or twice yearly. Ranges are not label-derived and vary substantially; the prescriber decides.
Monitoring
CBC, CMP, fasting glucose, and sleep or circadian self-report measures. There is no validated biomarker of benefit for this peptide — which is itself a reason for caution.
Cautions
Active malignancy, pregnancy or lactation, and any use in children. Given the evidence base, HelixCare clinicians frequently decline this request and redirect to interventions with real data.
Limited human dataRx · Compounded
16-amino-acid mitochondrial-DNA–encoded peptide from the 12S rRNA region.
MOTS-c
Mitochondrial signalling · Metabolic
A peptide encoded inside the mitochondrial genome itself. In cell and rodent models it inhibits the folate–methionine cycle, leading to accumulation of AICAR and activation of AMPK, with improved insulin sensitivity and protection against diet-induced obesity1. Under metabolic stress it translocates to the nucleus and participates in regulating nuclear gene expression, including antioxidant-response-element genes alongside NRF22. It is exercise-responsive and declines with age; in mice, treatment improved measures of age-dependent physical decline3.
Route
Subcutaneous injection.
Dose framework
5–10 mg SC, 1–3× per week in cycles — the range reported by clinics. No human dose-finding trial supports this.
Timing
Commonly 30–60 minutes before zone-2 or resistance training on training days; late-evening dosing avoided.
Monitoring
Fasting glucose and insulin with HOMA-IR, HbA1c, lipids and ApoB, hs-CRP, CMP; functional measures (VO₂max or six-minute walk, HRV, grip strength).
Cautions
Pregnancy or lactation, active malignancy, severe renal impairment (caution); unknown interaction profile with insulin-sensitising drugs — hypoglycaemia risk should be considered when combined. Prohibited in sanctioned sport as a non-approved substance.
A cell-permeable, mitochondria-targeted tetrapeptide that concentrates on the inner mitochondrial membrane and interacts with cardiolipin, the signature phospholipid of that membrane45. Preclinical work reports preserved cristae architecture and respiratory supercomplex organisation, improved electron-transport coupling, reduced electron leak and reactive oxygen species, and rapid improvement in mitochondrial energetics and exercise tolerance in aged mice67.
Clinically, elamipretide has been through randomised trials in primary mitochondrial myopathy8 and a phase 2/3 trial with open-label extension in Barth syndrome9; those programmes carried 40 mg/day subcutaneously. It has since received a narrow accelerated approval in the United States for Barth syndrome (marketed as Forzinity, 2025). Approval for one rare disease is not evidence for general anti-ageing use.
Route
Subcutaneous injection (daily in the trial programmes).
Dose framework
Trials used 40 mg SC daily. Off-label wellness protocols commonly start far lower — on the order of 5–10 mg/day, 5 days on / 2 off — a practice choice with no trial validation either way.
Timing
Morning dosing is conventional in these frameworks; consistency matters more than clock time.
Monitoring
CMP with renal function, CK, lactate and pyruvate, hs-CRP, GDF-15 and FGF-21 where available, plus functional testing (six-minute walk, VO₂max). Injection sites reviewed at every check-in.
Cautions
Injection-site reactions are the most commonly reported adverse effect in elamipretide trials. Avoid in pregnancy or lactation; caution in significant renal impairment; not studied in healthy-ageing populations. Prohibited in sanctioned sport.
These two are different in kind from the rest of the library: they are FDA-approved medicines with large randomised trials and published labels. HelixCare clinicians dose them to label, titrate against tolerance, and pair them with protein intake and resistance training to protect lean mass.
In the STEP 1 randomised trial of adults with overweight or obesity, once-weekly semaglutide 2.4 mg plus lifestyle intervention produced substantial, sustained weight loss versus placebo over 68 weeks16. Mechanistically it slows gastric emptying and acts on central appetite regulation via GLP-1 receptor signalling.
Dose framework (label titration)
0.25 mg once weekly to start, escalating stepwise at roughly four-week intervals toward the target of 2.4 mg weekly for chronic weight management, as tolerated. Titration slows or pauses for gastrointestinal side effects.
Route & storage
Subcutaneous, same day each week. Refrigerate; follow the dispensed product's in-use storage and beyond-use instructions exactly.
Monitoring
Weight and waist circumference, blood pressure, HbA1c and fasting glucose, lipids and ApoB, CMP with renal and hepatic function, lipase if pancreatitis is suspected; protein intake and lean-mass tracking; mood and eating-behaviour review.
Cautions
Contraindicated with a personal or family history of medullary thyroid carcinoma or MEN 2, and in pregnancy. Caution with history of pancreatitis, gallbladder disease, severe gastroparesis, diabetic retinopathy, and with insulin or sulfonylureas (hypoglycaemia risk — those doses usually need reducing). Compounded copies are a regulatory and safety concern; HelixCare dispenses approved product where available.
Dual GIP and GLP-1 receptor agonist · once-weekly subcutaneous.
Tirzepatide
Weight & metabolic · GIP / GLP-1
In SURMOUNT-1, once-weekly tirzepatide produced dose-dependent weight reduction over 72 weeks in adults with obesity or overweight without diabetes17. Its dual incretin mechanism engages both GIP and GLP-1 receptors.
Dose framework (label titration)
2.5 mg once weekly for four weeks, then increases of 2.5 mg every four weeks as tolerated toward maintenance doses of 5, 10 or 15 mg weekly.
Route & storage
Subcutaneous, same day each week; refrigerated per the dispensed product's instructions.
Monitoring
As for semaglutide: weight and body composition, HbA1c and fasting glucose, lipids and ApoB, blood pressure, renal and hepatic panels, gastrointestinal tolerance, protein intake and resistance-training adherence.
Cautions
Same class cautions: medullary thyroid carcinoma or MEN 2 history, pregnancy, pancreatitis history, severe gastrointestinal disease; dose reduction of concurrent insulin or sulfonylureas. Rapid weight loss without resistance training and adequate protein costs lean mass — that is a monitored endpoint, not an afterthought.
Thymosin α-1
Approved in some countries; not FDA-approved
A 28-amino-acid thymic peptide that modulates T-cell and dendritic-cell function. It is an approved medicine in a number of countries outside the United States (used adjunctively in hepatitis B and C and in some immune-compromised settings) and has a real clinical literature there; in the US it is not FDA-approved and is used off-label.
Framework
Subcutaneous; reported practice ranges around 0.8–1.6 mg given 2–3× weekly in cycles of 4–8 weeks.
Monitor
CBC with differential, CMP, hs-CRP; autoimmune review — immune activation can aggravate autoimmunity.
Cautions
Autoimmune disease, organ transplant or immunosuppression (may oppose therapy), pregnancy or lactation.
KPV
Preclinical-dominant
The C-terminal tripeptide of α-melanocyte-stimulating hormone (Lys-Pro-Val), studied preclinically for anti-inflammatory effects in colitis and skin models. It is used in practice for gut and dermatological inflammation, typically oral or topical rather than injected. Human controlled data are lacking.
Framework
Oral capsules (often enteric-coated for colonic delivery) or topical cream; reported ranges around 200–500 mcg daily in 4–8 week cycles. Subcutaneous use is less common.
Monitor
Symptom scores, hs-CRP, faecal calprotectin where a diagnosed inflammatory bowel condition is being co-managed by gastroenterology.
Cautions
Not a substitute for guideline IBD therapy. Pregnancy or lactation; unclear interaction profile with immunosuppressants.
Selank
Very limited data outside original research tradition
A synthetic heptapeptide analogue of the immunopeptide tuftsin, developed in Russia and studied there as an anxiolytic. Independent replication outside that literature is minimal. Presented here for completeness, not endorsement.
Framework
Intranasal drops or spray in short courses (days to a few weeks) in reported practice; dosing varies widely between sources.
Monitor
Validated anxiety and sleep instruments, blood pressure; screen for the psychiatric conditions that warrant evidence-based treatment instead.
Cautions
Never a substitute for assessment and treatment of an anxiety or mood disorder. Pregnancy or lactation; unknown interactions with psychotropics.
A note on the thin end of the library
Editorial
Four of the twelve monographs here rest on animal, cell or single-tradition human data. We keep them in the library because patients ask about them and deserve a straight answer — including, often, "the evidence does not support this, and here is what does." A HelixCare clinician declining to prescribe is the protocol working, not failing.
Dose ranges on this page are illustrative clinician protocol frameworks compiled from published labels and from practice patterns reported in the clinical literature and by practitioners. They are shown as reported, not endorsed, and are not a recommendation to self-administer. Final dosing, eligibility, cycle length and monitoring are determined by a licensed HelixCare Clinics prescriber for an individual patient.
Flagship protocol · HelixCare × Binary Helix Research
The Mitochondrial Renewal Protocol
MOTS-c × SS-31 · 12 weeks · clinician-supervised
Two peptides that act on mitochondria from opposite directions: one is a signal encoded by the mitochondrial genome, the other is a structural protectant of the inner membrane. We pair them, then measure — including a transcript panel we are using to test a hypothesis rather than to prove a claim.
One organelle · two branches
Branch A — MOTS-cthe signal
Branch B — SS-31the protectant
ConvergenceProposed
16Amino acids · MOTS-c
4Amino acids · SS-31
11mRNA panel transcripts
12Week measured cycle
Two mechanisms, one organelle.
Branch A · MOTS-c
A peptide the mitochondrion writes itself
MOTS-c is a 16-amino-acid peptide encoded within the mitochondrial genome, in the 12S rRNA region — a small open reading frame inside what was long read as structural RNA. In cell and rodent models it inhibits the folate–methionine cycle; AICAR accumulates as a consequence and AMPK, the cell's low-energy sensor, is activated. Downstream, the reported phenotype is improved insulin sensitivity, greater metabolic flexibility and protection against diet-induced obesity1.
Under metabolic stress, MOTS-c does something unusual for a mitochondrial product: it translocates to the nucleus, where it participates in the regulation of nuclear gene expression — including antioxidant response element (ARE) genes, alongside NRF22. This is the basis for calling it a retrograde signal from mitochondrion to nucleus.
MOTS-c is also exercise-induced and declines with age; in mice, treatment improved measures of age-dependent physical decline and muscle homeostasis3. Human interventional data remain limited — which is why the protocol below is framed as a monitored cycle, not a therapy.
Branch B · SS-31 (elamipretide)
A tetrapeptide that lives on the inner membrane
SS-31 is a cell-permeable, cationic tetrapeptide — D-Arg-Dmt-Lys-Phe-NH₂ — that crosses membranes without a transporter and concentrates on the inner mitochondrial membrane, where it interacts with cardiolipin, the unusual four-tailed phospholipid that organises that membrane45.
Binding cardiolipin is reported to preserve cristae architecture and the organisation of respiratory supercomplexes — the physical arrangement that lets electrons hand off efficiently. The consequences described in preclinical work: tighter electron-transport coupling, less electron leak and reactive oxygen species, better-maintained membrane potential, and reduction of the peroxidase activity cytochrome c acquires when cardiolipin is disordered — a step upstream of apoptotic signalling45.
In aged mice, SS-31 rapidly improved mitochondrial energetics and skeletal-muscle performance6 and reversed markers of age-related redox stress while improving exercise tolerance7. In humans it has been studied in primary mitochondrial myopathy8 and Barth syndrome9.
Both branches are drawn only as far as the published mechanisms go. The convergence node is labelled proposed deliberately: improved oxidative-phosphorylation efficiency is the plausible shared endpoint, not a demonstrated joint effect of the two peptides given together. No trial has tested this combination in humans.
Gene-level read-outs
NDUFS1 and COX5A: what we measure, not what we claim.
These two transcripts sit at the entry and the exit of the electron transport chain. That makes them useful instruments. It does not make them proven targets of either peptide.
A claim you may have seen elsewhere
Peptide marketing sometimes states that MOTS-c and SS-31 "optimise NDUFS1 and COX5A expression." That specific link is not established in the published literature, and we do not make it. What is established are the mechanisms described above: AMPK activation and NRF2-associated antioxidant gene regulation for MOTS-c12, and cardiolipin binding with preserved cristae and respiratory-supercomplex organisation for SS-3145. NDUFS1 and COX5A appear in our panel as monitored transcript read-outs in a hypothesis-driven study — we are testing whether a supervised MOTS-c × SS-31 cycle shifts them, and we will report what we find either way.
NDUFS1
Complex I · the entry point for electrons
NDUFS1 encodes the largest core iron–sulfur subunit of Complex I (NADH:ubiquinone oxidoreductase) — the first and largest complex of the respiratory chain, where electrons from NADH enter and are passed along a chain of Fe–S clusters to ubiquinone. Complex I is both the chain's gateway and one of its principal sites of superoxide production when electron flow stalls, which is why a Complex I subunit is the natural front-end instrument for a protocol aimed at electron leak.
Measured endpoint
COX5A
Complex IV · the terminal step
COX5A encodes a nuclear-encoded subunit of Complex IV (cytochrome c oxidase), the terminal enzyme of the chain, which takes electrons from cytochrome c and reduces molecular oxygen to water. Proton pumping by Complexes I, III and IV builds the electrochemical gradient that ATP synthase then spends to make ATP. Because COX5A is nuclear-encoded, it also reports on nuclear–mitochondrial coordination — the thing a retrograde signal like MOTS-c would be expected to touch, if it touches transcription at all.
Measured endpoint
Where the two monitored transcripts sit. SS-31's cardiolipin mechanism acts on the membrane environment that holds these complexes together; MOTS-c's mechanism is signalling — AMPK and, under stress, nuclear gene regulation. Whether either shifts these particular transcripts in humans is the open question this panel exists to answer.
Side by side, carefully worded
Comparison of MOTS-c and SS-31 across mechanism, Complex I and Complex IV relevance, and downstream effect
Feature
MOTS-c
SS-31 (elamipretide)
Primary established mechanism
Mitochondrial-DNA–encoded peptide; inhibits the folate–methionine cycle → AICAR accumulation → AMPK activation; translocates to the nucleus under metabolic stress and participates in nuclear gene regulation including ARE targets with NRF212.
Cell-permeable tetrapeptide that concentrates on the inner mitochondrial membrane and binds cardiolipin, preserving cristae architecture and respiratory-supercomplex organisation45.
Complex I (NDUFS1) relevance
Proposed, not demonstrated. An AMPK- and NRF2-associated route to mitochondrial biogenesis and antioxidant programmes could plausibly touch Complex I subunit expression. Direct regulation of NDUFS1 by MOTS-c has not been shown. NDUFS1 is a measured endpoint in our panel.
Indirect and structural. Cardiolipin-dependent preservation of supercomplex organisation concerns how Complex I sits and functions in the membrane, not how much NDUFS1 is transcribed. NDUFS1 is a measured endpoint, not a claimed target.
Complex IV (COX5A) relevance
Proposed, not demonstrated. COX5A is nuclear-encoded, so a retrograde mitochondrial-to-nuclear signal is a coherent hypothesis — and exactly that: a hypothesis. Measured endpoint.
Indirect and functional. Reduced cytochrome c peroxidase activity and better electron handoff concern Complex IV's working environment. No established transcriptional effect on COX5A. Measured endpoint.
Downstream effect reported in the literature
Improved insulin sensitivity and metabolic flexibility; protection against diet-induced obesity in rodents; improved measures of age-dependent physical decline in aged mice13.
Improved mitochondrial energetics and exercise tolerance in aged mice; reduced redox stress67; clinical evaluation in primary mitochondrial myopathy8 and Barth syndrome9.
Human evidence grade
Limited human data. No dose-finding or outcome trial supports wellness dosing.
Randomised human trials in rare mitochondrial disease; narrow accelerated approval for Barth syndrome (Forzinity, 2025). No trial support for healthy-ageing use.
Exploratory transcripts on the panel
Transcriptomic studies of ageing tissue consistently report broad, age-associated shifts that extend well beyond bioenergetics — including genes involved in synaptic transmission and WNT signalling. Four transcripts flagged in an ageing transcriptomic signature reviewed by our team are carried on our panel as exploratory, hypothesis-generating measures only. We are not citing a specific study for them, we make no claim that either peptide affects them, and we would not act clinically on a change in any of them.
Seven core transcripts (bioenergetics, biogenesis and antioxidant response) plus four exploratory transcripts. The exploratory set is reported back to participants as exploratory and is excluded from any dosing decision.
The derived protocol
Twelve weeks, four phases, one washout.
Sequence matters in the design logic: restore the membrane first, then add the signal. Every dose below is an illustrative framework for clinician discussion — the prescriber sets the actual numbers, and may decline the protocol entirely.
SS-31 · PrimeBH·RX-05
MOTS-c · SignalBH·RX-04
Weeks 0 → 12 · then 4–8 week washout
−2−1123456789101112
Phase 0 · BaselineWeeks −2 to 0
Labs · mRNA panel
Phase 1 · PrimeSS-31 daily AM · wks 1–4
SS-31 prime, mornings
SS-31 continues
Phase 2 · SignalMOTS-c 2–3×/wk · wks 3–12
MOTS-c 30–60 min pre-training, training days
Phase 3 · ConsolidateSS-31 taper · wks 9–12
Taper SS-31 · retest wk 12
Lifestyle co-factorsThroughout
Zone 2 150+ min/wk · resistance training · sleep · protein
Check-ins & labsWk 4 · wk 8 · wk 12 retest
Phase 0 · weeks −2 to 0
Baseline
Two weeks of measurement before anything is injected. No baseline, no protocol.
Membrane and cristae integrity first, on the reasoning that a better-organised inner membrane is a better substrate for any subsequent signal.
SS-31 subcutaneously, once daily in the morning. Clinician-chosen dose: trials used 40 mg/day89; many clinic protocols start considerably lower — for example 5–10 mg/day, 5 days on and 2 off.
Rotate injection sites; photograph and log any site reaction.
Week 4 check-in: tolerance, site reactions, CK and CMP if indicated.
No MOTS-c yet, so that any adverse effect has one candidate cause.
Phase 2 · weeks 3–12
Signal — add MOTS-c
Overlaps the end of Phase 1 deliberately, so the addition is stepwise rather than a fresh start.
MOTS-c subcutaneously, 2–3× per week — clinic frameworks commonly cite 5–10 mg per dose.
Dose 30–60 minutes before zone-2 or resistance training on training days. Rationale: MOTS-c is exercise-induced and acts through AMPK, so aligning it with an exercise stimulus is the mechanistically coherent choice13. This is design logic, not a proven timing effect.
Continue SS-31 through week 8 at the established dose.
Phase 3 · weeks 9–12
Consolidate & retest
Taper down, measure, and stop. The washout is part of the protocol, not an interruption of it.
Reduce SS-31 frequency (for example daily → 3× weekly → stop).
Continue MOTS-c to week 12 on the same training-aligned schedule.
Week 12: full retest of the Phase 0 panel, including the mRNA panel and functional measures.
Then a 4–8 week washout before any repeat cycle is even considered. Repeat cycles require a fresh clinician review.
Side effects reported
Injection-site reactions are the most commonly reported adverse effect in elamipretide clinical programmes — expect and monitor for them89.
Transient fatigue, flushing or palpitations are reported anecdotally with MOTS-c. These are practitioner and user reports, not trial findings.
Injection-related risks common to all subcutaneous peptides: bruising, local infection, sterile technique failures.
Sleep disturbance if dosed late in the day.
Contraindications & cautions
Pregnancy and lactation — do not use.
Active cancer — do not use; cancer history requires a documented specialist discussion first.
Severe renal impairment — caution; clearance and safety are not characterised in this population.
Significant hepatic impairment, uncontrolled cardiovascular disease, or an unstable medical condition — defer.
Insulin or sulfonylurea therapy — AMPK-directed mechanisms and hypoglycaemia risk require prescriber review of concurrent doses.
Prohibited in sanctioned sport. Both peptides are non-approved substances for this use and fall under the WADA Prohibited List; athletes must check the current list.
Stop and contact HelixCare
Stop dosing and contact your HelixCare clinician — or emergency services if symptoms are severe — for: chest pain, new or worsening shortness of breath, palpitations that do not settle; signs of allergic reaction (widespread rash, facial or throat swelling, wheeze); an injection site that becomes hot, spreading, purulent or acutely painful, or any fever; persistent vomiting or inability to keep fluids down; new severe headache or visual change; symptoms of hypoglycaemia (sweating, tremor, confusion) if you take insulin or a sulfonylurea; or any new symptom that worries you. Symptom reports logged in MyHelix are routed for clinician review, but MyHelix is not an emergency service.
Supportive co-factors
The lifestyle half of this protocol carries better evidence than the peptide half, and is not optional: 150+ minutes per week of zone-2 aerobic work, two or more resistance sessions, seven to nine hours of sleep, adequate protein (commonly 1.4–2.0 g/kg/day for training adults), and a consistent eating window — time-restricted eating is used here for adherence and circadian regularity rather than as a claimed mitochondrial intervention. A short list of nutrients with a mitochondrial rationale is offered alongside; evidence for each varies, and none is a substitute for the lifestyle base.
Ubiquinol (CoQ10)
Electron carrier between Complexes I/II and III; the clearest mechanistic rationale of the group, strongest evidence in statin-associated myalgia and primary CoQ10 deficiency.
Mitophagy and NAD⁺ pathways are plausible and actively researched; human outcome evidence is early. Magnesium supports ATP-dependent enzymes and is worth correcting if intake or status is low.
The Mitochondrial Renewal Protocol is an illustrative clinician protocol framework and an internal research design, not a treatment recommendation and not a validated therapy. MOTS-c is investigational and not FDA-approved; elamipretide's US approval is limited to Barth syndrome and does not extend to healthy-ageing use. Compounding availability varies by jurisdiction. Final dosing, eligibility, monitoring and any decision to prescribe rest with a licensed HelixCare Clinics prescriber. Both peptides are prohibited in sanctioned sport under the WADA Prohibited List.
Build the profile a HelixCare clinician needs: genome, biomarkers, medications and goals — held in your wallet, shared on your terms, with re-test reminders built in.
Citations below support mechanism and clinical-trial statements in the text. Protocol frameworks, practice-reported dose ranges and monitoring panels are not derived from these papers and are cited to no one — they are clinical-practice summaries and internal study design.
Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015;21(3):443–454.
Kim KH, Son JM, Benayoun BA, Lee C. The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. Cell Metab. 2018;28(3):516–524.
Reynolds JC, Lai RW, Woodhead JST, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021;12:470.
Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. Br J Pharmacol. 2014;171(8):2029–2050.
Birk AV, Liu S, Soong Y, et al. The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol. 2013;24(8):1250–1261.
Siegel MP, Kruse SE, Percival JM, et al. Mitochondrial-targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice. Aging Cell. 2013;12(5):763–771.
Campbell MD, Duan J, Samuelson AT, et al. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice. Free Radic Biol Med. 2019;134:268–281.
Karaa A, Haas R, Goldstein A, et al. Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy. Neurology. 2018;90(14):e1212–e1221.
Thompson WR, Hornby B, Manuel R, et al. A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome. Genet Med. 2021;23(3):471–478.
Seiwerth S, Rucman R, Turkovic B, et al. BPC 157 and standard angiogenic growth factors. Gastrointestinal tract healing, lessons from tendon, ligament, muscle and bone healing. Curr Pharm Des. 2018;24(18):1972–1989.
Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JH. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol. 2011;110(3):774–780.
Goldstein AL, Hannappel E, Sosne G, Kleinman HK. Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opin Biol Ther. 2012;12(1):37–51.
Philp D, Kleinman HK. Animal studies with thymosin β4, a multifunctional tissue repair and regeneration peptide. Ann N Y Acad Sci. 2010;1194:81–86.
Pickart L, Margolina A. Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. Int J Mol Sci. 2018;19(7):1987.
Pickart L, Vasquez-Soltero JM, Margolina A. GHK peptide as a natural modulator of multiple cellular pathways in skin regeneration. Biomed Res Int. 2015;2015:648108.
Wilding JPH, Batterham RL, Calanna S, et al. Once-weekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021;384(11):989–1002.
Jastreboff AM, Aronne LJ, Ahmad NN, et al. Tirzepatide once weekly for the treatment of obesity. N Engl J Med. 2022;387(3):205–216.
Medical and regulatory disclaimer. This page is educational and is not medical advice, a prescription, or an offer to supply prescription medicines. Nothing here should be used to self-administer any peptide. Many of the peptides described are investigational and are not approved by the FDA for the uses discussed; where an approval exists (semaglutide, tirzepatide, and elamipretide for Barth syndrome) we name the specific indication, and an approval for one indication is not evidence for another.
Dosing. All dose ranges are illustrative clinician protocol frameworks — compiled from approved labels and from practice patterns reported in the clinical literature and by practitioners, shown as reported rather than endorsed. Final dosing, eligibility, cycle length and monitoring are determined by a licensed HelixCare Clinics prescriber for an individual patient after review of history, medications and laboratory data.
Compounding and availability. Prescription peptides are dispensed only where legally permitted, through licensed 503A and 503B compounding pharmacy partners or as approved products. Availability of any given substance varies by jurisdiction and by regulatory status; some substances discussed here — BPC-157 among them — face specific compounding restrictions in the United States and may be unavailable through legitimate channels.
Sport. Several substances on this page, including BPC-157, thymosin β4 fragments, growth-hormone secretagogues, MOTS-c and SS-31, are prohibited in sanctioned sport under the World Anti-Doping Agency Prohibited List. Athletes subject to testing must consult the current list and their anti-doping authority before any use.
Emergencies. If you experience severe or worsening symptoms, seek urgent medical care. MyHelix messaging is reviewed by clinicians during service hours and is not an emergency service.