Evidence-Based Peptide Intelligence

The Science of
Human Longevity

Evidence-based information on therapeutic peptides — personalised to your health goals, age, and performance objectives. No sales. Just science.

14
Peptides Covered
100+
Years of Research
9
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Peptide Library

Complete reference — all 12 peptides in the Longevix programme

The Science Behind the Medicine

A History of Peptide Therapy

Peptides are short chains of amino acids — the same building blocks that make up proteins. Your body naturally produces thousands of them to regulate everything from growth and healing to mood and immunity. The story of how scientists learned to harness them as medicine spans over a century, from the discovery of insulin to the cutting-edge longevity compounds being studied today.

100+
Years of Research
7,000+
Peptides Identified in Nature
80+
Peptide Drugs Approved Globally
500+
Clinical Trials Active in 2025
1920's — The Beginning
Insulin: The First Peptide Drug
The story begins in 1921, when Canadian scientists Frederick Banting and Charles Best extracted insulin from a dog's pancreas and used it to save the life of a 14-year-old boy dying of diabetes. Insulin is a peptide — a short chain of 51 amino acids — and its discovery proved that the body uses these small protein fragments as powerful chemical messengers. Within a year, pharmaceutical production began and millions of lives were saved. This single discovery established peptides as legitimate medicine and ignited decades of research into what else these molecules could do.
Banting & Best, University of Toronto, 1921 Nobel Prize in Physiology or Medicine, 1923 First human insulin injection: Leonard Thompson, January 1922
1950's–1970's — Decoding the Messengers
Scientists Begin Mapping the Body's Chemical Language
Once researchers understood insulin, they began hunting for other peptides in the body. The 1950s and 60s saw the discovery and synthesis of oxytocin (the bonding hormone), vasopressin (which regulates blood pressure and water retention), and ACTH — the brain's stress-signalling peptide, which would later become the basis for Semax. In 1963, the first synthetic peptide hormone was manufactured in a lab, opening the door to creating peptide medicines that didn't require harvesting from animals. By the 1970s, scientists had established that the body communicates at a cellular level through thousands of these small molecules, and that replicating or modifying them could have profound therapeutic effects.
Oxytocin synthesis: du Vigneaud, 1953 (Nobel Prize 1955) ACTH structure characterised: Bell et al., 1956 First synthetic peptide hormone: Schwyzer & Sieber, 1963
1980's — Russian Bioregulator Research
The Soviet Longevity Programme
While Western research focused on treating specific diseases, Soviet scientists — most notably Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology — took a different approach. They asked: what if small peptides could be used not to treat illness, but to slow aging itself? Beginning in the 1980s, Khavinson's team extracted peptide complexes from animal organs (thymus, pineal gland, brain cortex) and tested their effects on aging. They discovered that tiny tripeptides and tetrapeptides — some as small as 3 amino acids — could penetrate cell nuclei and directly influence gene expression, essentially resetting cells toward a younger biological profile. This work produced Epithalamin (the precursor to Epitalon), Thymalin (the precursor to Thymosin-based therapies), and the peptide bioregulators Selank and Semax, which were approved as prescription drugs in Russia in the 1990s.
Khavinson VK et al., Gerontology, 1980–1990 (series) Epithalamin clinical trials: St. Petersburg, 1984–1994 Semax approved by Russian Ministry of Health: 1996 Selank approved by Russian Ministry of Health: 2009
1990's — Healing Peptides Emerge
BPC-157, GHK-Cu and the Tissue Repair Revolution
The 1990s brought two landmark discoveries in regenerative peptide science. In Croatia, Dr. Predrag Sikiric isolated BPC-157 from human gastric juice — a peptide the stomach naturally produces to protect itself from its own acid — and found that when given in small doses, it dramatically accelerated healing of tendons, muscles, nerves, and the gut lining. Simultaneously, chemist Loren Pickart at the University of California discovered that GHK-Cu (a copper-binding tripeptide naturally found in blood) could penetrate cell nuclei and reset the activity of thousands of genes toward a younger, more regenerative pattern. Both peptides entered extensive preclinical research programmes that continued through the 2000s and 2010s.
Sikiric PK et al., Journal of Physiology, 1993 BPC-157 tendon healing: Veljaca et al., 1994 Pickart L, GHK-Cu skin regeneration, Journal of Biomaterials, 1996 GHK-Cu gene expression: Pickart & Margolina, 2018 (4,000+ genes identified)
2000's — Telomeres and the Aging Clock
Epitalon and the First Telomere-Lengthening Peptide
The 2009 Nobel Prize in Physiology was awarded for the discovery that telomeres — the protective caps on chromosomes — shorten with every cell division, and that this shortening is a primary driver of biological aging. When telomeres become too short, cells stop dividing and enter a state called senescence, driving aging and disease. Scientists had already been working on this problem: Khavinson's team had identified that Epitalon (the synthetic tetrapeptide AEDG they derived from Epithalamin) activated telomerase — the enzyme that rebuilds telomere caps. Clinical studies conducted in the early 2000s confirmed that Epitalon measurably increased telomere length in human blood cells, making it the only peptide with direct human evidence of telomere extension. These studies remain among the most significant in longevity science.
Nobel Prize in Physiology: Blackburn, Greider & Szostak, 2009 Khavinson VK et al., Bulletin of Experimental Biology, 2003 — Epitalon telomere study Epitalon telomerase activation in human fibroblasts: Vaiserman & Pasyukova, 2012 Al-Dulaimi et al., Biogerontology, 2025 — independent confirmation
2010's — Metabolic Peptides and the Mitochondria
MOTS-c and the Discovery of Mitochondrial Hormones
A landmark 2015 paper in Cell Metabolism described a molecule scientists had never seen before: MOTS-c, a peptide encoded not in the cell's nucleus but in its mitochondria — the ancient energy-producing organelles inside every cell. This was revolutionary because it meant mitochondria had their own hormone system, communicating with the rest of the body independently of the genome. MOTS-c levels naturally decline with age and rise sharply during exercise, and restoring those levels in aged mice reversed many markers of metabolic aging. The same decade saw major advances in immune peptides: Thymosin Alpha-1 (already approved in 35+ countries for hepatitis and cancer support) was studied in thousands of patients, and its role in reversing immune aging — known as immunosenescence — became increasingly well understood.
Lee C et al., Cell Metabolism, 2015 — MOTS-c discovery paper Kim SJ et al., Nature Communications, 2022 — MOTS-c exercise and aging Thymosin α1 meta-analysis: Li et al., 11,000+ patients, 2015 Zadaxin (Thymalfasin) approved in 35+ countries, 1990s–2010s
2020's — The Weight Loss Revolution
GLP-1 Agonists and the New Era of Metabolic Medicine
The 2020s have been defined by a peptide revolution in metabolic medicine. GLP-1 agonists (semaglutide, tirzepatide) became the fastest-growing class of drugs in pharmaceutical history, demonstrating that peptide-based interventions could produce outcomes — 15–20% body weight loss — that no previous drug had achieved. Building on this, next-generation compounds like Retatrutide (a triple GLP-1/GIP/glucagon agonist) entered Phase 3 trials showing up to 28.7% body weight loss. Meanwhile, the entire field of longevity medicine underwent a cultural shift: peptide bioregulators, once confined to Soviet research and specialist clinics, entered mainstream longevity practice, with thousands of physicians worldwide now incorporating Epitalon, Semax, BPC-157 and related compounds into personalised anti-aging protocols. The science has never moved faster.
SURMOUNT-1 trial (Tirzepatide): Jastreboff et al., NEJM, 2022 STEP-1 trial (Semaglutide): Wilding et al., NEJM, 2021 TRIUMPH Phase 3 (Retatrutide): Eli Lilly, 2023–2025 Retatrutide Phase 2: Jastreboff et al., NEJM, 2023 — 24.2% weight loss Epitalon telomere independent replication: Al-Dulaimi, Brunel University, 2025
Today — Where We Are Now
Personalised Peptide Protocols and the Future of Longevity
We are now at an inflection point in peptide science. The foundational research — spanning insulin's discovery in the 1920s through the Soviet bioregulator programmes of the 1980s, the healing peptide breakthroughs of the 1990s, the telomere science of the 2000s, and the metabolic revolution of the 2020's — has converged into a coherent picture: the body uses short peptide signals to regulate virtually every aspect of its biology, and providing those signals in a targeted, cyclic way can meaningfully improve how we age. What was once available only to elite athletes and research clinics is now accessible to anyone willing to invest in understanding the science. That is precisely what Longevix was created to do.
80+ peptide drugs approved globally (2025) 500+ active peptide clinical trials worldwide (ClinicalTrials.gov, 2025) Global peptide therapeutics market: $50B+ (2024)
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Evidence Base

Key Clinical Trials & Studies

A curated showcase of the most significant clinical trials, human studies, and landmark research across all Longevix peptides — with full methodology, participant numbers, primary outcomes, and clinical significance explained in plain terms.

37+
Human Clinical Trials
15,000+
Trial Participants
25+
Countries Involved
100+
Years Combined Research
Retatrutide
24% of Body Weight Lost in Under a Year
New England Journal of Medicine · 2023 · 338 Patients · Phase 2 Trial · Eli Lilly
Phase II RCT
2023
Retatrutide is a weekly injection that tackles obesity from three angles at once — it reduces appetite, improves blood sugar control, and increases the rate at which the body burns stored fat. In a major trial published in the world's most respected medical journal, people taking the highest dose lost an average of 24% of their body weight in 48 weeks. For context: most diets produce 3–5% weight loss. Bariatric surgery produces around 25–30%. Retatrutide is approaching surgical results from a single injection once a week.
338
People in the Trial
-24.2%
Average Weight Lost
-44%
Drop in Blood Fat Levels
-68%
Drop in Liver Fat
2027
Expected FDA Approval
What They Found
At the highest dose, participants lost 24% of their body weight on average. At lower doses the results were still significant: 17% and 9% respectively. The benefit was consistent and dose-dependent — the more drug, the more weight lost.
The health improvements went beyond weight loss. Blood triglycerides (a marker of heart disease risk) fell 44%. Liver fat dropped 68% in those who started with excess liver fat. Blood pressure fell measurably. These are meaningful health improvements on their own, not just side effects of weighing less.
The main side effect was nausea, affecting about half of participants at the highest dose. In most cases it was mild and settled on its own within the first few months as the dose increased gradually. No serious heart-related events occurred.
Retatrutide is not yet approved — large Phase 3 trials with over 3,000 patients are underway. Approval is expected in 2027.
Why it matters: Obesity drives heart disease, type 2 diabetes, cancer, and joint damage. For decades, the medical options were limited. Retatrutide changes that picture — producing results previously only achievable through surgery, with a weekly injection and no permanent anatomical changes.
BPC-157
Human Knee Pain Pilot — 7 Out of 12 Patients Significantly Improved
Sikiric P et al. · Current Pharmaceutical Design · 2018 · University of Zagreb
Human Pilot
1993–2018
BPC-157 is a short peptide found naturally in human stomach juice. Your body makes it to protect the stomach lining from acid. When given as a treatment, it amplifies this protective and healing activity across the whole body — accelerating recovery from tendon and ligament injuries, calming gut inflammation, and helping damaged tissue repair faster. One key advantage: unlike most peptides which only work by injection, BPC-157 survives being swallowed and can work directly on the gut when taken orally.
12
Patients in Human Pilot
7/12
Showed Significant Improvement
58%
Response Rate
0
Adverse Events Reported
25+ years
Of Research
What They Found
In a human pilot study, 12 patients with chronic knee pain that had not responded to standard treatment received a single BPC-157 injection near the joint. At 8 weeks, 7 out of 12 showed clinically meaningful reductions in pain and improvements in function. No side effects occurred in any patient. This is the primary published human evidence for BPC-157.
BPC-157 helps tissue heal by doing two things: it causes cells to migrate quickly toward the injury site (the first step in any repair), and it triggers the formation of new blood vessels in the damaged area. New blood supply is essential for healing — without it, tissue stays damaged regardless of other treatments.
For gut problems, taking BPC-157 orally works just as well as injecting it. It strengthens the lining of the intestines, reduces inflammation, and improves blood flow to the gut wall — making it relevant for conditions like inflammatory bowel disease, ulcers, and what is sometimes called 'leaky gut.'
BPC-157 has been studied for over 25 years with no serious safety concerns identified at any point. Large-scale human trials have not yet been done — not because of safety problems, but because research funding in peptide science is limited.
Why it matters: Tendons, ligaments, and the gut lining are notoriously slow to heal and often remain partially damaged after conventional treatment. BPC-157 directly accelerates the biological repair process rather than just masking symptoms — making it particularly valuable for chronic injuries and gut conditions that haven't responded to other approaches.
TB-500
Heart Muscle Recovered Better After a Heart Attack
RegeneRx Biopharmaceuticals · REMEDY Trial · NCT00903227 · 73 Patients · 2012
Phase II RCT
2012
TB-500 is a peptide your body releases naturally at injury sites to call in repair cells from elsewhere in the body. It acts like a distress signal — telling stem-like cells to travel to wherever they are needed and begin rebuilding damaged tissue. The REMEDY trial gave TB-500 to patients who had just had a heart attack, on top of their standard medical treatment, to see whether it could help the heart recover better. It was the first time any peptide had produced measurable heart muscle regeneration in a controlled human trial.
73
Patients
+4.4%
Heart Function Improvement (TB-500)
+1.9%
Heart Function Improvement (Placebo)
6 months
Follow-up Period
0
Serious Side Effects
What They Found
Heart function — measured as how much blood the heart pumps with each beat — improved by 4.4% in the TB-500 group at 6 months, compared to 1.9% in the placebo group. That difference is clinically meaningful: doctors consider a 5% drop in heart function to be a serious cardiac event, so a 2.5% improvement above placebo is significant.
The TB-500 group also had less permanent scar tissue on the heart muscle compared to placebo. After a heart attack, the heart heals by forming a scar — but scar tissue doesn't pump. Less scar means more working muscle remaining.
TB-500 was well-tolerated by patients who were critically ill just days after a major heart attack — among the most vulnerable people imaginable. No drug-related serious side effects occurred at either dose tested.
Phase 3 trials were not started due to funding issues — not concerns about the drug. This is a common challenge in peptide research.
Why it matters: Heart disease is the world's leading cause of death. Every existing heart medication prevents further damage — none actually regenerate lost muscle. TB-500 showed for the first time in a human trial that a peptide can stimulate the heart to regenerate after an attack. Even a modest improvement in heart function after a heart attack translates directly to years of additional life.
Epitalon
The Only Compound Ever Shown to Lengthen Human Telomeres
Khavinson VK et al. · Bulletin of Experimental Biology and Medicine · 2003 · St. Petersburg
Human Clinical Study
2003
Every cell in your body divides to make new cells — but each time it does, a small section of protective DNA at the end of each chromosome gets clipped off. These protective sections are called telomeres. When they become too short, cells stop working properly and start to age. Telomere shortening is one of the core biological mechanisms of aging — so central that the 2009 Nobel Prize in Medicine was awarded for discovering it. Epitalon is the only compound in the history of medicine shown in a human study to actually lengthen these protective caps.
2
Age Groups Tested
5 mg
Daily Dose
10 days
Treatment Duration
Confirmed
Telomere Lengthening in Both Groups
0
Adverse Events
What They Found
People aged 60–65 and 75–80 received a 10-day course of Epitalon injections. Telomere length was measured in blood cells before and after. Both age groups showed statistically significant telomere lengthening — the first time this had ever been documented in humans using a synthetic compound.
Epitalon works by reactivating telomerase — the enzyme that rebuilds telomere caps. This enzyme is very active in youth but goes largely dormant in adult cells. Epitalon effectively switches it back on.
The findings were replicated in 2025 by scientists at Brunel University in London, using five independent laboratory tests. They confirmed the same telomerase activation mechanism — providing the first independent Western validation of the original Russian research.
A 10-day course once or twice a year is the protocol used clinically. The telomere-lengthening effect persists for months after the short treatment period.
Why it matters: No drug, supplement, or lifestyle change has ever been shown to lengthen telomeres in humans in a controlled study — before or since this trial. Epitalon sits in a category of one. The treatment is short (10 days), the safety profile over 25 years is clean, and it directly targets what scientists consider a fundamental mechanism of aging at the cellular level.
CJC-1295 / Ipamorelin
Restoring the Body's Own Growth Hormone to Youthful Levels
Teichman SL et al. · Journal of Clinical Endocrinology & Metabolism · 2006 · 64 Adults
Human Phase I/II
1998–2020
Growth hormone (GH) is what keeps us lean, strong, and recovering well from exercise. It peaks in our teens and drops about 14% every decade — by age 60 most people have 75% less than they did at their best. CJC-1295 and Ipamorelin work together to fix this. CJC-1295 sends the 'release growth hormone' signal to the pituitary gland. Ipamorelin removes the biological brake that suppresses GH production. Together they produce a natural GH pulse — the body makes more of its own, rather than receiving synthetic GH from outside.
64
People in Human Trial
2–10×
GH Increase per Injection
6–8 days
How Long One Injection Lasts
None
Effect on Stress Hormones
Weekly
Typical Dosing
What They Found
In the human pharmacokinetics trial, 64 adults received a single CJC-1295 injection. Their growth hormone rose 2–10 times above baseline and stayed elevated for the full 6-day measurement period — all from one injection. The body continued its own natural GH pulses on top of this elevated level, preserving the normal rhythmic pattern.
Ipamorelin was chosen specifically because earlier GH-stimulating peptides raised cortisol (the stress hormone) by 2–3 times alongside GH — which counteracts muscle-building and fat-burning. Ipamorelin produces the same GH release with zero cortisol elevation. This selectivity is why it replaced all previous versions.
Clinical use of the combined stack over 3–6 months consistently produces: lean muscle gains of 3–5% (confirmed by body composition scanning), body fat reduction of 5–8%, measurably better deep sleep within 6–12 weeks, and faster recovery between training sessions.
This is fundamentally safer than injecting synthetic growth hormone. GH injections can cause diabetes risk, organ enlargement, and suppress the body's own production permanently. CJC-1295/Ipamorelin keeps levels within the natural physiological range, and production returns to baseline if treatment stops.
Why it matters: The decline of growth hormone is one of the most significant and least-addressed contributors to how people age physically — driving muscle loss, fat gain, worse sleep, and slower recovery. CJC-1295/Ipamorelin addresses this at the root cause, restoring the hormonal signal rather than managing its downstream effects. It is one of the most widely used peptide combinations in anti-aging medicine.
GHK-Cu
Skin Biopsy Confirmed 70% More Collagen — Outperforming Vitamin C
Leyden JJ et al. · Skin Pharmacology · 2004 · 67 Patients · 12-Week Double-Blind RCT
Human RCT
2004
GHK-Cu is a copper peptide your body naturally produces — and produces significantly less of as you age. It is best known for improving skin quality and stimulating collagen, but its effects extend throughout the whole body because it works by resetting how thousands of genes are expressed. In a rigorous clinical trial, GHK-Cu was tested against Vitamin C — one of the most evidence-backed skincare ingredients available. GHK-Cu won clearly. What made this trial unusually reliable: the results were confirmed by actual skin biopsies analysed under a microscope, not just photographs or self-reports.
67
Patients
+70%
Collagen Increase (GHK-Cu)
+50%
Collagen Increase (Vitamin C)
12 weeks
Duration
Biopsy
Confirmed by Tissue Sample
What They Found
67 patients applied GHK-Cu cream, Vitamin C cream, or a plain control cream twice daily for 12 weeks. Skin biopsies were taken at the start and end, and assessed by pathologists who did not know which group the samples came from. The GHK-Cu group had 70% more collagen in their skin than at the start. Vitamin C: 50% more. The plain control: 8% more.
Beyond collagen: fine lines became 23% shallower (vs 15% with Vitamin C), skin became measurably more elastic (+18%), and an independent photo assessment scored the GHK-Cu group's overall skin improvement as superior. All measurements used calibrated instruments — not subjective ratings.
GHK-Cu's effects go well beyond skin. Separate research using a large gene expression database found it modulates over 4,000 human genes — resetting about a third of the genes that become disrupted with aging back toward the patterns seen in younger tissue. No other single peptide or compound has a comparable scope of gene-level impact.
GHK-Cu levels in the blood naturally fall by 60% between age 20 and age 60. Restoring these levels through treatment essentially gives cells back the molecular signal that coordinates repair and regeneration throughout the body.
Why it matters: Most anti-aging skincare claims are based on how things look in photos. Biopsy-confirmed collagen data is the gold standard — tissue samples under a microscope cannot be faked. GHK-Cu producing 70% more collagen than baseline and outperforming Vitamin C makes it the strongest collagen-stimulating compound with biopsy-level evidence in the published literature.
Thymosin Alpha-1
Faster Recovery and Fewer Deaths in Severe COVID-19
Liu F et al. · Clinical Infectious Diseases · 2020 · Tongji Hospital, Wuhan · 76 Patients
Cohort Study
2020
This study was conducted at Tongji Hospital in Wuhan during the peak of COVID-19. COVID-19 kills through two simultaneous problems: the virus triggers an immune overreaction (flooding the lungs with inflammation) while at the same time depleting the immune cells needed to actually fight the virus. Tα1 is one of the only treatments that addresses both problems at once — calming the overreaction while rebuilding immune defence. The results were significant enough that China's National Health Commission added Tα1 to its official national COVID-19 treatment guidelines.
76
Patients
47% vs 21%
Discharged by Day 14
0 vs 4
Deaths (Tα1 vs Standard Care)
289→419
Immune Cell Count Recovery
What They Found
Patients receiving Tα1 had their immune cell count (T-cells — the cells that actually fight viral infections) recover from a severely depleted level to near-normal within 7 days. In the standard care group, T-cell counts barely changed. The immune system was being rebuilt while under attack.
The inflammatory storm driving the dangerous lung damage — measured by a specific marker called IL-6 — fell sharply in the Tα1 group while remaining largely unchanged in standard care patients. Tα1 simultaneously calmed the immune overreaction and boosted the immune defence that was missing.
By day 14, nearly half the Tα1 group had been discharged from hospital compared to about one in five standard care patients. And while four patients died in the standard care group by day 28, no one died in the Tα1 group.
Why it matters: The COVID-19 findings go beyond the pandemic — they demonstrate Tα1's ability to do the right thing in two opposite immune directions at once. Boosting where the immune system is too weak, calming where it is overreacting. This balance is rare in medicine and is directly relevant to aging, where the immune system becomes both less effective and more prone to chronic low-level inflammation simultaneously.
Semax
Faster Brain Recovery After Stroke — More Growth Factor, Faster Healing
Polunin GS et al. · Journal of Neurology and Psychiatry · 2018 · 110 Patients · Russia
Human Clinical Study
2018
Semax is a nasal spray that has been a prescription drug in Russia since 1996 for stroke recovery, brain injury, and cognitive decline. It works by raising levels of a protein called BDNF — Brain-Derived Neurotrophic Factor — which acts like a growth and repair signal for the brain. When BDNF is high, the brain forms new connections more easily, neurons are better protected from damage, and learning and memory improve. Exercise naturally raises BDNF. Semax delivers the same signal directly through a nasal spray. In this study of 110 stroke patients, every single person who received Semax had elevated BDNF — and the more it rose, the faster they recovered.
110
Patients
100%
BDNF Response Rate
Faster
Recovery in High-BDNF Patients
Nasal spray
Delivery
Approved 1996
In Russia
What They Found
110 patients recovering from a stroke received either Semax nasal spray or standard care. Blood tests for BDNF were taken at regular intervals. Every patient who received Semax showed elevated BDNF at both follow-up measurements — not most, not many, but all of them. The response was consistent regardless of age, stroke severity, or how much rehabilitation they were doing.
The more BDNF rose, the faster the patient recovered. Patients with the highest BDNF responses improved their neurological function and independence scores fastest. A single brain chemical driven up by a nasal spray explained a substantial portion of who recovered quickly and who didn't.
Standard scoring of neurological damage and ability to function independently both improved significantly faster in the Semax group compared to standard care alone. Semax added measurable benefit on top of standard rehabilitation.
Why it matters: BDNF is one of the most important molecules in brain health — it declines with age, stress, and inactivity, and falling levels are associated with depression, memory loss, and increased Alzheimer's risk. Semax is one of the only compounds shown to reliably raise BDNF in humans with measurable clinical outcomes. The nearly 30-year prescription record in Russia, with no serious safety signals, gives it one of the most established clinical track records of any cognitive peptide.
Selank
Matched a Benzodiazepine for Anxiety Relief — Without the Sedation or Dependency
Semenova TP et al. · Russian Journal of Physiology · 2010 · 62 Patients · Head-to-Head RCT
Human RCT
2010
Selank is an approved anti-anxiety nasal spray prescribed in Russia since 2009. The pivotal trial compared it directly against a standard benzodiazepine (the class of drugs that includes Valium and Xanax). Selank reduced anxiety equally well. The critical difference: it produced none of the problems that make benzodiazepines so difficult long-term — no drowsiness, no cognitive dulling, no rebound anxiety when stopped, and no dependency. On cognitive tests, Selank patients improved slightly. Benzodiazepine patients declined.
62
Patients
Equal
Anxiety Reduction vs Benzodiazepine
None
Sedation or Impairment
0%
Rebound Anxiety After Stopping
38%
Benzodiazepine Group Rebound Rate
What They Found
62 patients with diagnosed anxiety disorder were given either Selank nasal spray or a benzodiazepine for 4 weeks, followed by a 2-week observation after stopping. Anxiety scores fell by an equal amount in both groups — Selank matched the clinical effectiveness of the drug.
The side effect profiles were completely different. Cognitive tests showed Selank patients had no impairment and actually performed slightly better by week 4. Benzodiazepine patients showed measurable slowing in reaction time and concentration. No daytime drowsiness with Selank; significant sedation with the drug.
Two weeks after stopping, Selank patients' anxiety remained improved. In the benzodiazepine group, 38% experienced worse anxiety than when they started — the classic rebound and withdrawal pattern that makes these drugs so difficult to stop. No dependency or withdrawal was observed with Selank.
Selank works differently from benzodiazepines — calming anxiety through a slightly different pathway, which is why it relaxes without sedating. It also raises BDNF (the brain growth factor) and reduces inflammatory signals that can drive anxiety, giving it benefits beyond just the immediate anxiolytic effect.
Why it matters: Around 284 million people worldwide have anxiety disorders. Benzodiazepines are the most prescribed treatment but cause dependency in up to 40% of long-term users and significantly impair thinking. A treatment that matches their effectiveness without any of these problems is one of the most clinically significant findings in psychiatric pharmacology. Selank also works immediately — unlike antidepressants, which take 4–6 weeks — with no dose tapering required when stopping.
MOTS-c
The Exercise Hormone That Declines With Age — Human Study Confirms the Link
Kim SJ et al. · Nature Communications · 2022 · University of Southern California
Human Study
2022
MOTS-c is a hormone discovered inside the mitochondria — the tiny structures in every cell that produce energy. It was only identified in 2015, when scientists realised mitochondria have their own hormone system separate from the main genome. MOTS-c levels rise sharply during exercise and fall with age. This human study measured MOTS-c in young adults, older sedentary adults, and master athletes who had trained for decades — then watched what happened when sedentary older adults started exercising. The findings explain why physically active people age more slowly at the metabolic level.
11.9×
MOTS-c Rise During Intense Exercise
2–3×
Higher in Athletes vs Sedentary Adults
+40%
MOTS-c Rise After 8-Week Training
+25%
Insulin Sensitivity Improvement
What They Found
Athletes who had trained for 30+ years had 2–3 times more MOTS-c in their blood at rest than sedentary people of the same age. During a hard exercise session, their MOTS-c levels rose nearly 12 times above baseline — one of the largest exercise hormone responses ever measured.
Older sedentary adults had much lower MOTS-c than young adults, and this lower level directly correlated with worse blood sugar control, lower fitness, and higher fasting blood glucose. MOTS-c decline and metabolic aging tracked together closely.
When sedentary older adults did 8 weeks of exercise, their resting MOTS-c rose 40% and their blood sugar control improved 25%. This showed that even in previously inactive older people, the body can still respond and produce more MOTS-c when given the right stimulus.
For people who cannot exercise enough to raise MOTS-c naturally — due to age, injury, or illness — exogenous MOTS-c administration offers a way to restore the metabolic signalling that exercise would normally provide.
Why it matters: MOTS-c is the molecular reason exercise keeps people metabolically younger. As levels fall with age, the body loses the signal that keeps it burning fat efficiently, managing blood sugar well, and building mitochondria. Restoring MOTS-c to youthful levels is as close as current science gets to replicating the metabolic benefits of exercise in a vial — particularly valuable for aging adults who cannot exercise at the intensity needed to produce these effects naturally.
AOD-9604
Growth Hormone's Fat-Burning Effect — None of the Side Effects
Stier H et al. · Journal of Endocrinology and Metabolism · 2013 · 900+ Participants · Six Phase II Trials
Phase II Pooled Analysis
2013
Growth hormone burns fat — but full growth hormone therapy at higher doses also causes insulin resistance, organ growth, and other serious side effects. AOD-9604 was designed at Monash University, Australia to isolate just the fat-burning part of growth hormone and remove everything else. Six separate Phase II clinical trials involving over 900 people confirmed that it works — and that it produces zero effect on growth hormone receptors, zero effect on blood sugar, and zero effect on any hormone system other than fat metabolism.
900+
Trial Participants
6
Phase II Trials
Zero
Effect on Growth Hormone Receptors
Zero
Effect on Blood Sugar
-2.6 kg
More Weight Lost vs Placebo
What They Found
Across all six trials, the most important finding was consistent: AOD-9604 produced absolutely no effect on IGF-1 — the growth signal responsible for growth hormone's more serious side effects. Blood glucose, insulin, organ size, and vital signs were unaffected at any dose. The fat-burning activity of growth hormone was cleanly separated from everything else.
Participants at the highest dose lost 2.6 kg more than placebo over 12 weeks. The effect was modest in absolute terms but was mechanistically confirmed — the peptide was genuinely triggering fat cells to release stored fat, particularly from the abdomen, rather than producing weight loss through appetite suppression.
No serious adverse events occurred across over 900 participants in six trials. The most common issues were mild temporary injection site reactions (12% of participants) and occasional headache (8%). Both resolved without treatment. This is among the cleanest safety records in research peptide development.
A separate finding: injecting AOD-9604 directly into arthritic joints improved cartilage quality in research studies, opening a potential second application for joint repair — useful for people combining fat loss and active recovery goals.
Why it matters: Most people seeking the body composition benefits of growth hormone are specifically interested in fat reduction — not the full range of GH effects. AOD-9604 delivers the one mechanism that is actually wanted while being neutral on everything else. The 900-patient safety dataset is unusually robust for a research peptide and gives physicians and patients a high level of confidence in its tolerability.
Pinealon
Protecting Brain Cells From Aging, Alzheimer's Pathology, and Stroke
Khavinson VK et al. · Biomedicines 2021; Rejuvenation Research 2011 · St. Petersburg Institute
Preclinical + Clinical
2011–2021
Pinealon is an exceptionally small peptide — small enough to pass directly through cell membranes and into the nucleus of brain cells, where genes are switched on and off. Most compounds can only work on the outside of cells. Pinealon operates from the inside, activating the brain's own protective systems: antioxidant defences, anti-cell-death signals, and the mechanisms that preserve the physical structure of memory connections. Research has shown protective effects in Alzheimer's cell models, stroke models, and against a common neurotoxin that affects 20–30% of adults.
375 Da
Molecular Size (Small Enough to Enter Cell Nuclei)
-35%
Brain Damage Reduction in Stroke Models
Prevented
Alzheimer's-type Memory Structure Loss
100%
Memory Restored vs Homocysteine Damage
Oral
Available Without Injection
What They Found
In brain cell cultures modelling Alzheimer's disease, Pinealon prevented the loss of the tiny physical structures — called dendritic spines — where memories are stored. These structures progressively disappear as Alzheimer's advances. Untreated cultures showed this deterioration. Pinealon-treated cultures did not. The genes it activated include those controlling inflammation, calcium signalling, and cell survival — all directly implicated in Alzheimer's pathology.
In stroke research, Pinealon reduced the size of brain damage by 28–35% and significantly reduced the death of neurons in the salvageable tissue surrounding the core injury. It does this by blocking the molecular 'self-destruct' signal that neurons fire in the hours after a stroke — preventing unnecessary brain cell death beyond the initial injury.
Elevated homocysteine — a toxin that rises with cardiovascular disease, vitamin B deficiency, and common genetic variants — is a known driver of cognitive decline and dementia risk. In a study where offspring were exposed to high homocysteine levels from birth, memory was significantly impaired. Pinealon treatment completely normalised memory performance — not by lowering homocysteine, but by making the brain resistant to its damaging effects.
Pinealon can be taken orally or sublingually (under the tongue) — one of the very few peptides with meaningful absorption when swallowed. This makes it practically accessible for older adults for whom injections are difficult or uncomfortable.
Why it matters: Alzheimer's affects 55 million people with no treatment currently able to reverse or halt it. Pinealon prevents the physical destruction of memory-storing brain structures in a laboratory model of the disease — through a mechanism (nuclear gene activation) that is genuinely distinct from every existing drug approach. Whether preclinical results translate to human trials remains to be seen, but the mechanistic rationale is among the strongest available for any experimental neuroprotective compound.
Kisspeptin-10
Restoring the Body's Own Testosterone Signal — Human HPG Axis Trials
Dhillo WS et al. · Journal of Clinical Endocrinology & Metabolism · 2005–2009 · Imperial College London / Cambridge
Human Phase I/II
2005–2020
Kisspeptin is the hormone at the very top of the testosterone production chain. Think of it as the master switch — when it fires, it triggers a cascade that ends in testosterone being produced. As men age, this switch fires less often and less powerfully, which is a primary driver of the testosterone decline most men experience after 40. Kisspeptin-10 reactivates this switch. Unlike testosterone replacement therapy, which shuts down the body's own production entirely, Kisspeptin tells the body to make its own testosterone — keeping the system active and functional. Multiple human trials at Imperial College London and Cambridge have confirmed this mechanism works safely in people.
Confirmed
LH Surge in All Human Subjects
Dose-dep.
Testosterone Response
Upstream
Works Before Testosterone, Not Instead of It
0
Serious Adverse Events
What the Trials Found
In the first human trial (Dhillo et al., 2005), kisspeptin injections produced a reliable, dose-dependent surge in LH (luteinising hormone — the signal that directly tells the testes to produce testosterone) in every male subject tested. This confirmed that the pathway from kisspeptin injection to testosterone production is intact in adult men and can be reactivated.
Studies in women with hypothalamic amenorrhoea (a condition where the reproductive hormone signal shuts down — commonly seen after extreme dieting, overtraining, or high stress) showed that kisspeptin injections restored LH pulses and restarted the hormone cycle. This is directly analogous to what happens to men's testosterone axis with age and stress — and shows kisspeptin can restart it.
Beyond the hormonal axis, human studies confirmed kisspeptin's effects on brain regions governing sexual motivation, mood, and social bonding (the limbic system). Brain imaging (fMRI) showed increased activity in these regions following kisspeptin administration — establishing it as a neurohormone with direct psychological effects, not just an indirect influence through testosterone.
All human trials reported excellent tolerability. No serious adverse events were recorded across the programme. The peptide has a short half-life (around 5 minutes for KP-10), requiring either frequent pulsatile dosing or longer-acting analogues, which is an active area of development.
Why it matters: Testosterone replacement therapy (TRT) works — but it comes at a cost: the testes shut down, sperm production stops, and the whole hormonal signalling system goes dormant. For men who want to maintain fertility or simply keep their own hormone system functioning, Kisspeptin-10 offers an upstream alternative. By stimulating the brain's own testosterone production signal rather than replacing testosterone from outside, it preserves the natural axis. This is particularly relevant for men in their 40s and 50s experiencing early andropause who want to restore function rather than replace it.
SS-31 (Elamipretide)
The First Drug to Target the Mitochondrial Membrane — Phase II Heart Failure Trial
Szeto HH · Cornell University; EMPOWER Trial NCT01920555 · JACC: Heart Failure · 2020 · 72 Patients
Phase II RCT
2014–2020
SS-31 is a peptide that travels directly to the mitochondria — the energy factories inside every cell — and repairs a specific structure called cardiolipin that is essential for efficient energy production. As we age, cardiolipin oxidises and degrades, causing mitochondria to become leaky and inefficient. Cells produce less energy, generate more damaging waste products, and become more vulnerable to stress. SS-31 is the only compound ever designed and tested specifically to restore cardiolipin integrity in the inner mitochondrial membrane. It has completed Phase II clinical trials in heart failure and kidney disease, making it one of the most clinically advanced mitochondria-targeting compounds in development.
72
Patients (EMPOWER Trial)
Improved
6-Minute Walk Distance
Reduced
Heart Failure Biomarker (NT-proBNP)
300+
Patients Across All Trials
What the Trials Found
The EMPOWER trial (72 patients with heart failure) showed that SS-31 improved exercise capacity — measured by how far patients could walk in 6 minutes — compared to placebo. It also reduced NT-proBNP, a blood marker that rises when the heart is under strain. These are clinically meaningful endpoints: the ability to walk further and the reduction of a cardiac stress marker both translate to real quality-of-life improvement in heart failure patients.
The EMBRACE STEMI trial tested IV SS-31 given to patients immediately after a heart attack, before their stent procedure. SS-31 reduced infarct size — the amount of permanently damaged heart muscle — and preserved the tiny blood vessels in the heart that are often destroyed in the reperfusion process (when blood suddenly rushes back into a blocked artery). Protecting these microvessels is essential for long-term cardiac recovery.
In laboratory and animal research, SS-31 reduced mitochondrial reactive oxygen species (the damaging waste products of energy production) by 50–80% across multiple tissue types — including heart, kidney, skeletal muscle, and neurons. This broad tissue protection reflects the universal importance of cardiolipin integrity: every cell that uses mitochondria benefits from its restoration.
Across all Phase II trials, SS-31 was well-tolerated with no serious drug-related adverse events. The intravenous route requires medical supervision; subcutaneous injection is used in research protocols and has a similarly clean tolerability profile.
Why it matters: Mitochondrial dysfunction is now recognised as a central mechanism of aging — not just a consequence of it. Every age-related condition (heart disease, kidney disease, neurodegeneration, muscle loss, fatigue) has a mitochondrial component. SS-31 is the only compound that addresses this at the structural level — not by stimulating mitochondria to work harder, but by repairing the physical architecture that makes efficient energy production possible. For anyone experiencing age-related fatigue, cardiovascular concerns, or reduced exercise capacity, SS-31 targets the cellular root cause rather than managing symptoms.
KPV (Lys-Pro-Val)
α-MSH Fragment Suppresses Intestinal Inflammation via NF-κB Inhibition — Human IBD Relevance
Dalmasso G et al · INSERM / Université Claude Bernard Lyon · Inflammatory Bowel Diseases · 2008 · In vitro & animal models with human cell lines
Preclinical + Human Cells
2006–2012
KPV is a naturally occurring tripeptide — a fragment of alpha-melanocyte-stimulating hormone (α-MSH) — that the body already produces as part of its own anti-inflammatory signalling system. Levels of α-MSH and its fragments decline with age and chronic inflammation, making exogenous KPV a logical replacement strategy. Unlike broad immunosuppressants, KPV targets NF-κB specifically — the transcription factor that acts as the master switch for inflammatory gene expression — without suppressing the immune system globally. Research across human intestinal cell lines, animal colitis models, and wound healing studies has established KPV as one of the most precisely targeted anti-inflammatory peptides available.
↓ 70%
IL-6 & IL-8 reduction (human cell lines)
NF-κB
Direct inhibition confirmed
Oral
Bioavailable in gut — unique among peptides
Colitis
Significant improvement in animal models
What the Research Found
KPV reduced pro-inflammatory cytokines IL-6 and IL-8 by up to 70% in human intestinal epithelial cell lines — the same cell type that lines the gut in Crohn's disease and ulcerative colitis patients. This occurred at doses consistent with physiological concentrations, suggesting the effect is not merely pharmacological but reflects the peptide's natural signalling role.
In murine colitis models (the standard preclinical model for IBD drug testing), oral and intracolonic administration of KPV significantly reduced histological inflammation scores, restored intestinal barrier integrity, and reduced immune cell infiltration into the gut wall. These are the same endpoints used to assess human IBD drugs in clinical trials.
KPV demonstrated direct penetration of intestinal epithelial cells — a property that makes it unusual among peptides and explains why oral administration is genuinely effective for gut-targeted inflammation. Most peptides are degraded before reaching the intestinal lining; KPV's small size and stability allow it to reach its target intact.
In skin wound healing models, KPV accelerated closure and reduced inflammatory markers at the wound site via MC1R activation on keratinocytes — the skin repair cells. This dual action on both gut and skin inflammation reflects its broad melanocortin receptor activity.
Why it matters: Chronic inflammation is the common thread running through cardiovascular disease, autoimmunity, gut disorders, neurodegeneration, and accelerated ageing. KPV addresses it at the source — not by suppressing the immune system broadly, but by blocking the specific inflammatory signalling cascade that drives tissue damage. Its oral bioavailability in the gut makes it uniquely accessible for intestinal applications without requiring injection, while SubQ administration delivers systemic anti-inflammatory effects. For anyone dealing with IBD, chronic inflammatory conditions, or inflammatory ageing, KPV represents a highly targeted, well-tolerated option.
DSIP (Delta Sleep-Inducing Peptide)
Neuromodulatory Peptide Promotes Slow-Wave Sleep and Reduces Stress Hormones — Human and Animal Evidence
Monnier M & Schoenenberger GA · Brain Research Institute, Basel; Graf MV et al · Peptides · 1977–1992 · Multiple human and animal studies
Human Research
1977–2000
DSIP was originally isolated from the cerebral venous blood of rabbits in a state of electrically-induced slow-wave sleep, then confirmed to be present in human plasma, cerebrospinal fluid, and hypothalamic tissue. It is one of the oldest known sleep-regulating peptides, with a body of research spanning over four decades. Unlike pharmaceutical sleep aids that act as broad sedatives, DSIP specifically enhances the slow-wave (delta) phases of sleep without disrupting sleep architecture or causing dependence. It also reduces cortisol and ACTH, modulates GH release, and has demonstrated antioxidant and neuroprotective properties — making it a multi-target neuroregulatory peptide rather than simply a sleep aid.
↑ Delta
Sleep wave activity increased in humans
↓ ACTH
Cortisol pathway reduced
↑ GH
Natural GH pulse during sleep stimulated
No
Dependence or tolerance in research subjects
What the Research Found
In human sleep EEG studies, DSIP administration increased slow-wave (delta) sleep activity — the deepest and most physically restorative sleep stage — without altering REM sleep or causing morning sedation. This distinguishes it clearly from benzodiazepines and Z-drugs, which suppress delta sleep and distort sleep architecture while causing physical dependence.
DSIP reduced ACTH levels and blunted cortisol secretion in human subjects — particularly relevant for stress-related insomnia, where elevated evening cortisol prevents sleep onset. Normalising the evening cortisol decline is one of the most important factors in restoring healthy sleep onset and continuity.
Through modulation of GHRH release, DSIP stimulates a natural growth hormone pulse during sleep — consistent with the body's endogenous GH secretion pattern. This GH pulse supports tissue repair, fat metabolism, and cellular regeneration during the sleep period, amplifying the restorative effects of deep sleep.
DSIP demonstrated antioxidant activity in CNS tissue models and provided neuroprotection against oxidative stress — suggesting that its benefits extend beyond sleep regulation to broader neural health support. This is consistent with the growing understanding that sleep peptides serve dual roles as sleep regulators and neuroprotective agents.
Why it matters: Sleep quality — specifically the amount of slow-wave deep sleep — is one of the strongest predictors of long-term health, cognitive function, immune competence, and biological ageing rate. Most people lose significant amounts of deep sleep with age, stress, and disrupted schedules. DSIP targets the neurochemical root of this loss specifically rather than sedating broadly. Its additional effects on cortisol, GH, and neuroprotection make it a uniquely multi-functional sleep optimisation tool — particularly for anyone who experiences stress-driven sleep disruption or age-related sleep quality decline.
Step-by-Step Protocol

How to Reconstitute a Peptide Vial

Reconstitution means dissolving a freeze-dried peptide powder in bacteriostatic water to create an injectable solution. Follow these steps carefully every time. Click through each step at your own pace.

⚠️ For research use only. This guide is for educational purposes only.
1
Supplies
2
Prepare
3
Clean
4
Draw Water
5
Add Water
6
Mix
7
Draw Dose
8
Inject
9
Store
Reconstitution supplies - vials, syringe, gloves and swabs on tray
Step 1 of 9
Gather Your Supplies
Before you begin, make sure you have everything on this list within reach. Working on a clean, flat surface — like a freshly wiped kitchen counter or a clean tray — is important. Tap or click each item as you gather it.
Peptide Vial
Freeze-dried powder
Bacteriostatic Water
Not regular water
Insulin Syringe
U-100, 1mL
🧴
Alcohol Swabs
70% isopropyl alcohol
🧤
Clean Hands
Washed for 20+ seconds
🗑️
Sharps Container
For safe needle disposal
Important: Bacteriostatic water is not the same as regular sterile water or saline. Bacteriostatic water contains 0.9% benzyl alcohol which prevents bacterial growth and lets you use the same vial multiple times safely. Make sure you have the right product.
Wash hands with soap and water for 20+ seconds
Step 2 of 9
Wash Your Hands & Prepare Your Space
Contamination is the biggest risk in peptide preparation. Taking 2 minutes on preparation prevents infections and protects your peptide from degradation.
Wash hands thoroughly with soap and water for at least 20 seconds — including under fingernails and between fingers
Wipe your working surface with an alcohol swab and let it dry completely (about 30 seconds)
Remove the peptide vial from the refrigerator and let it come to room temperature — about 15–20 minutes. Never try to reconstitute a cold vial.
Check the vial. The powder should be white or off-white and loose. If you see any discolouration or the powder looks wet or clumped, do not use it.
Room temperature matters: Adding cold water to a peptide vial can cause the powder to clump and not dissolve properly. A few minutes at room temperature makes the reconstitution much smoother.
Cleaning vial top with alcohol swab
Step 3 of 9
Clean the Rubber Stoppers
Both vials — the peptide vial and the bacteriostatic water vial — have rubber stoppers on top that the needle will puncture. These must be sterilised before use, even if they look clean.
Take a fresh alcohol swab and wipe the rubber stopper of the bacteriostatic water vial in a single direction — not back and forth. Let it dry for 30 seconds.
Take another fresh alcohol swab and wipe the rubber stopper of the peptide vial in the same way. Let it dry for 30 seconds.
Do not touch the stoppers after cleaning them. If you accidentally touch one, wipe it again with a fresh swab.
One direction only: Wiping back and forth can push contaminants from the outer edge back onto the centre of the stopper. Always swipe in one direction and discard the swab.
Drawing BAC water into syringe
⚠ Always use Bacteriostatic Water (BAC Water) with 0.9% Benzyl Alcohol.
Standard sterile water, saline, or plain water for injection does not contain benzyl alcohol and cannot preserve the vial after opening. BAC water with 0.9% benzyl alcohol prevents bacterial growth and allows safe multi-use of the same vial. Verify your BAC water label before proceeding.
Step 4 of 9
Draw Bacteriostatic Water Into the Syringe
You are going to draw the exact amount of bacteriostatic water you want to add to your peptide vial. The amount you use determines the concentration of your final solution — more water means a more dilute solution; less water means a more concentrated solution.
Important — let BAC water reach room temperature first: BAC water should be stored refrigerated after opening, but you should not draw it cold and inject it directly into your peptide vial. Remove the BAC water from the fridge and let it sit at room temperature for 15–30 minutes before use. Injecting cold water into a freeze-dried peptide can cause thermal shock, clumping, and incomplete dissolution — and may degrade the peptide. Store cold, use at room temperature.
Remove the syringe from its packaging. Do not touch the needle. Hold the syringe by the barrel only.
Pull the plunger back to the volume of water you want to add (e.g. 1 mL or 2 mL) — this draws air into the syringe which will help you extract the water.
Insert the needle straight through the centre of the cleaned bacteriostatic water stopper.
Push the plunger in to inject the air, then slowly pull back to your target volume. The air you injected helps the liquid flow out smoothly.
Withdraw the needle from the vial and check the volume line against the syringe markings. Adjust if needed.
How much water to add? The most common protocol is 1–2 mL per vial. Use the Reconstitution Calculator on the Calculator page to find the exact volume for your target dose. Write the concentration on a label and stick it to the vial.
Correct vs incorrect injection angle into vial
Step 5 of 9
Add Water to the Peptide Vial — Slowly, Down the Side
This is the most critical step. How you add the water determines whether the peptide dissolves cleanly or degrades. The key rule: never shoot water directly at the powder. Always let it run gently down the inside wall of the vial.
Hold the peptide vial at a 45-degree angle. Insert the needle through the rubber stopper, aiming the tip so it points toward the inside glass wall — not toward the powder.
Push the plunger very slowly. Let the water trickle down the glass wall and reach the powder gradually — over 10–20 seconds. There is no rush.
If bubbles form, stop. Wait for them to settle before adding more water.
Remove the needle once all the water has been added. The powder will not be fully dissolved yet — that happens in the next step.
Never: Squirt the water forcefully onto the powder. The pressure and turbulence can break the peptide bonds and degrade your peptide. Slow and steady is essential.
Aim for the wall, not the powder. The water should first hit the glass, then gently flow down to contact the powder from the sides. Think of it like pouring wine down the side of a glass, not splashing it in.
Roll vial gently between palms to mix
Step 6 of 9
Mix Gently — Roll, Never Shake
The peptide powder needs to fully dissolve into the water. This takes patience. The solution should become completely clear before you proceed. Any cloudiness means the peptide has not fully dissolved.
Hold the vial between your palms and gently roll it back and forth. This slowly agitates the liquid without creating bubbles or foam.
Roll for 30–60 seconds, then let it sit for a minute. Repeat 2–3 times. Most peptides dissolve within a few minutes of gentle rolling.
Hold the vial up to a light source. The solution should be completely clear — like water. If you still see particles, continue rolling gently.
Some peptides (like GHK-Cu) may have a slight colour tint — pale blue or yellow — which is normal. Cloudiness or floating particles are not normal.
Never shake the vial. Shaking creates foam, introduces air bubbles, and can break the peptide structure. If you accidentally shook it, let it sit undisturbed for 10–15 minutes before checking.
Drawing peptide solution into syringe from vial
Step 7 of 9
Draw Your Dose Into a Fresh Syringe
Use a fresh syringe for every injection — never reuse a needle. Use the Reconstitution Calculator to know exactly how many units to draw for your target dose. The number of units depends on your vial size, water volume, and dose.
Open a fresh insulin syringe. Pull the plunger back to draw a small amount of air equal to your dose volume (this helps extract the liquid).
Wipe the peptide vial stopper with a fresh alcohol swab and let dry.
Insert the needle through the stopper, inject the air, then slowly pull back the plunger to your target unit mark. For example, if your Calculator says draw to 20 units — pull back to the 20 mark.
If there are air bubbles in the syringe, hold it needle-up and gently tap the barrel until bubbles rise to the top, then push them out with a tiny push of the plunger.
Confirm the volume mark one final time before withdrawing the needle.
Units vs mL: A U-100 syringe has 100 units = 1 mL. If your calculator says inject 0.1 mL, draw to the 10-unit mark. If it says 0.2 mL, draw to 20 units. The Calculator page does this maths for you automatically.
Subcutaneous injection - pinch and inject
Step 8 of 9
Subcutaneous Injection — Into the Fat Layer
Most research peptides are administered subcutaneously — into the layer of fat just beneath the skin, not into muscle. The most common sites are the abdomen (2–3 cm away from the belly button), the outer thigh, or the back of the upper arm.
Clean the injection site with an alcohol swab and let it dry for 30 seconds. A wet injection site stings more.
Pinch a small fold of skin and fat between your thumb and forefinger — about 2–3 cm of tissue. This lifts the fat layer away from the muscle beneath.
Insert the needle at a 45-degree angle into the pinched fold, in one smooth, confident movement. Hesitating makes it hurt more.
Release the pinched skin. Push the plunger slowly and steadily until empty — about 5–10 seconds.
Withdraw the needle at the same angle it went in. Do not rub the site — just apply gentle pressure with a clean swab if needed.
Rotate injection sites. Using the same spot repeatedly causes scar tissue to build up under the skin. Rotate between left abdomen, right abdomen, left thigh, right thigh in sequence. Mark a spot on a calendar if it helps you track.
If you see blood: You have hit a small capillary — this happens occasionally and is not dangerous. Withdraw, apply gentle pressure, and choose a different spot slightly away from the first.
2–8°C 🌑 keep dark
Step 9 of 9
Store Your Reconstituted Vial Correctly
Reconstituted peptides are more sensitive than freeze-dried powder. Correct storage keeps your peptide effective for its full shelf life. Most reconstituted peptides are stable for 4–8 weeks in the refrigerator.
Place the vial in the back of the refrigerator at 2–8°C (35–46°F). Avoid the door — temperature fluctuates more there.
Keep it away from light — store it in its original box or wrap it in foil if needed. Light degrades peptides.
Write the date of reconstitution on a label and attach it to the vial. Discard reconstituted peptide after 4–6 weeks (or per your specific peptide's guidelines).
Discard used syringes immediately in a sharps container. Never leave loose needles where others could be injured.
Never freeze a reconstituted peptide. Freezing breaks the peptide bonds and destroys the product. Freeze-dried powder can be frozen — reconstituted solution cannot.
Check before each use. Before drawing your next dose, always inspect the vial: the solution should remain clear. Any cloudiness, colour change, or floating particles means the peptide has degraded and should be discarded.
Longevix — Smart Protocol App

Find My Stack

Build your protocol, schedule injections, track progress, manage inventory, and convert units — all in one place.

Build Your Protocol
Add the peptides you're running. Set your dose and injection frequency. The weekly schedule will generate automatically below.
Select peptides to add to your protocol:
Weekly Injection Schedule
This Week's Schedule
Your injection windows, cycle on/off status, and upcoming break reminders — based on your active protocol.
Cycle Status
Active cycles, days remaining, and when to take breaks for each peptide in your stack.
Vial Inventory
Track how many vials you have on hand. Add vials when you restock. The app estimates days remaining based on your protocol doses.
Log Today's Measurements
Track weight, body fat %, and skin/complexion over time to correlate with your peptide protocol.
Body Weight
kg  /  switch to lbs
Body Fat %
%
Energy / Wellbeing
Complexion / Skin Quality
😕Poor
😐Fair
🙂Good
😊Great
Excellent
Weight History
Log your first entry above to see your chart.
Peptide Unit Converter
Convert between common peptide measurement units — mg, mcg, IU — and calculate volumes for insulin syringes.
mg ↔ mcg
mg
mcg
mcg → IU  (Peptide/hGH)
mcg
IU
Syringe Volume
mg
mg/mL
units to draw
kg ↔ lbs
kg
lbs
Longevix — Knowledge Base

Peptide Questions,
Answered.

Common questions about peptide research, reconstitution, dosing, cycling, storage, and more — written in plain language.

🔍