The WellSpry Peptide Intelligence Primer

CJC-1295 + Ipamorelin

Your physician looks for these patterns in your panel before introducing this protocol:

• ▸IGF-1 below optimal range for age (men: <150 ng/mL age 40+; women: <100 ng/mL age 40+)
• ▸Testosterone (total or free) trending low — compounding the lean mass risk
• ▸Body composition data showing lean mass percentage declining at 90-day retest
• ▸Fasting insulin elevated (>8 µIU/mL) indicating insulin resistance that GH optimisation can address
• ▸Subjective sleep quality declining alongside low AM cortisol (indicating disrupted cortisol rhythm, not excess)
• ▸Active GLP-1 use creating caloric deficit that risks muscle catabolism

Selank

Your physician looks for these patterns before introducing Selank:

• ▸Morning cortisol elevated (>18–20 µg/dL) — indicating HPA axis hyperactivity
• ▸DHEA-S low relative to age range — the cortisol:DHEA ratio is a key marker of chronic stress load
• ▸SHBG elevated — cortisol excess suppresses testosterone through SHBG upregulation; Selank addresses the upstream driver
• ▸Patient-reported anxiety, brain fog, or mood instability during GLP-1 adaptation
• ▸Thyroid markers in range but patient reporting fatigue and cognitive symptoms — cortisol dysregulation as the unexplained driver

Body Protection Compound 157 is a pentadecapeptide derived from a protein found in human gastric juice. It has been studied extensively in animal models for its cytoprotective and tissue-regenerative properties. BPC-157 promotes angiogenesis (new blood vessel formation), upregulates growth factor expression including VEGF and EGF, and modulates the nitric oxide system — all mechanisms that support tissue repair. Its gastric origin gives it particular affinity for gut mucosal healing, but its effects extend to tendon, ligament, muscle, and neural tissue.

• ·Gut lining integrity — the most evidence-supported application; directly relevant to GLP-1 patients experiencing GI side effects
• ·Leaky gut and intestinal permeability
• ·Tendon and ligament repair — connective tissue healing
• ·Inflammatory bowel conditions — modulation of gut inflammation
• ·Muscle injury recovery
• ·NSAID-induced gut damage reversal
• ·Neural regeneration — early research suggests neuroprotective properties

BPC-157 has over 100 published peer-reviewed studies, primarily in rodent models, demonstrating consistent tissue-healing and gut-protective effects. Human clinical trials are limited but ongoing. The mechanism is well-characterised. WellSpry prescribes it in clinical context — with documented gut dysbiosis or systemic inflammation from BIOHM and blood panel data — not as a general wellness supplement.

Oral capsule for gut-specific applications; subcutaneous injection for systemic tissue repair. Physician determines route, dose, and duration based on BIOHM score, hs-CRP, and specific symptoms. Typical course: 8–12 weeks with retest at 90 days.

TB-500 is a synthetic fragment of Thymosin Beta-4, a naturally occurring peptide found in virtually all human and animal cells. It promotes actin upregulation — actin being the protein that forms the structural basis of cell movement and repair. TB-500 enhances cell migration to injury sites, promotes new blood vessel formation, reduces inflammation at the injury site, and accelerates tissue remodelling. Unlike BPC-157 which is primarily gut-centric, TB-500's effects are more systemic — connective tissue, cardiac tissue, and neural tissue are all targets.

• ·Connective tissue repair — tendons, ligaments, fascia
• ·Muscle fibre repair following injury or intense training
• ·Flexibility and range of motion — actin regulation affects connective tissue compliance
• ·Systemic inflammation reduction
• ·Cardiac tissue protection — Thymosin Beta-4 has cardiac protective properties in research settings
• ·Hair growth — preliminary data suggests follicle support
• ·Often stacked with BPC-157 for comprehensive tissue repair

TB-500 is derived from a well-studied endogenous peptide. Animal and in vitro research supports its tissue-healing and anti-inflammatory effects. It is widely used in veterinary medicine for equine tendon injuries, where its efficacy is established. Human data is preliminary but mechanistically consistent.

Subcutaneous injection, typically 2x per week during loading phase (4–6 weeks), then weekly maintenance. Often prescribed alongside BPC-157 as a combined repair protocol.

AOD-9604 is a modified fragment of human growth hormone (hGH176-191) — specifically the C-terminal fragment responsible for hGH's fat-metabolising properties, without the growth-promoting or insulin-desensitising effects of full-length GH. It stimulates lipolysis (fat cell breakdown) and inhibits lipogenesis (fat storage) through beta-3 adrenergic receptor activation. Unlike GH itself, AOD-9604 does not raise IGF-1, does not cause insulin resistance, and does not stimulate cell proliferation — making it a targeted metabolic tool rather than a systemic hormone.

• ·Visceral fat reduction — particularly relevant for metabolic syndrome patients
• ·Plateau-breaking in GLP-1 weight loss — when medication-driven loss stalls, AOD-9604 targets the lipolytic mechanism independently
• ·Metabolic efficiency without GH side effects
• ·Cartilage repair — secondary mechanism; AOD-9604 has shown chondroprotective properties
• ·Fat loss without lean mass loss — the targeted mechanism avoids the muscle catabolism risk of systemic GH

AOD-9604 received FDA GRAS (Generally Recognized as Safe) designation for use as a food ingredient — a distinction that reflects a well-characterised safety profile at therapeutic doses. It completed Phase 2 clinical trials for obesity treatment. Its mechanism is well-understood as a targeted fragment of an extensively studied hormone.

Subcutaneous injection, typically daily, timed before exercise where possible. Physician determines dose based on insulin resistance markers and body composition data.

KPV is a tripeptide (Lysine-Proline-Valine) — the C-terminal fragment of alpha-melanocyte stimulating hormone (α-MSH). It exerts potent anti-inflammatory effects in intestinal tissue by inhibiting NF-κB — the master regulator of the inflammatory cascade — within gut epithelial cells and macrophages. Unlike systemic anti-inflammatories, KPV acts locally in the gut mucosa, making it highly targeted with minimal systemic effects. It also modulates the gut-brain axis through its MSH lineage, influencing satiety and appetite signalling.

• ·Intestinal inflammation — highly specific gut anti-inflammatory action
• ·Inflammatory bowel conditions — Crohn's, colitis, IBD-type presentations
• ·Gut dysbiosis-driven systemic inflammation — addresses the gut source rather than the downstream markers
• ·GLP-1 GI side effects — nausea, cramping, bloating driven by mucosal irritation
• ·Often stacked with BPC-157 for comprehensive gut repair (BPC-157 heals the lining; KPV reduces the inflammation)
• ·Satiety signalling — MSH pathway influence on appetite

KPV's anti-inflammatory mechanism in intestinal tissue is supported by multiple peer-reviewed studies demonstrating NF-κB inhibition in colonic epithelial cells. Its small size (tripeptide) allows for effective oral delivery — unusual for peptides, which are typically injected. This makes it practically accessible for gut-specific applications.

Oral capsule — one of the few peptides effectively delivered orally due to its small size. Typically prescribed alongside BPC-157 as a combined gut repair protocol. Physician determines dose and duration based on BIOHM score and inflammatory markers.

MOTS-C is a mitochondrial-derived peptide — encoded not in nuclear DNA but in the mitochondrial genome itself. It regulates nuclear gene expression through the AMPK pathway (the cell's master energy sensor), improves insulin sensitivity, and enhances skeletal muscle glucose uptake independently of insulin. MOTS-C levels decline with age and with metabolic dysfunction. Its effects have been described as 'exercise in a peptide' — it activates many of the same metabolic pathways triggered by physical exercise, including mitochondrial biogenesis.

• ·Mitochondrial function and energy production
• ·Insulin sensitivity — AMPK activation improves glucose disposal
• ·Fat loss plateau — particularly for patients with mitochondrial dysfunction or metabolic adaptation
• ·Exercise performance and tolerance — particularly in patients deconditioned from rapid weight loss
• ·Metabolic flexibility — ability to switch between fat and glucose as fuel
• ·Longevity — mitochondrial health is a primary driver of biological age

MOTS-C was first identified in 2015 and is one of the most actively researched peptides in the longevity field. Studies in rodent models demonstrate significant improvement in insulin sensitivity, exercise capacity, and metabolic flexibility. Human data is emerging. Its mitochondrial origin and AMPK mechanism are well-characterised.

Subcutaneous injection, typically 3–5x per week, timed before exercise where possible. Physician determines frequency based on metabolic markers and patient activity level.

Semax is a synthetic heptapeptide analogue of ACTH(4-7), developed by the Institute of Molecular Genetics of the Russian Academy of Sciences. It upregulates BDNF (brain-derived neurotrophic factor) and its receptor TrkB, enhances dopaminergic and serotonergic neurotransmission, and has neuroprotective effects against ischaemic and oxidative stress. It is approved as a pharmaceutical in Russia for ischaemic stroke recovery and cognitive disorders. Unlike stimulants, Semax enhances cognition through neurotrophic mechanisms rather than by elevating catecholamines — meaning no crash, no dependence, and sustainable effects.

• ·Cognitive clarity, focus, and working memory
• ·Brain fog — particularly relevant for GLP-1 patients in caloric deficit, where cognitive function often temporarily declines
• ·Stress resilience — BDNF upregulation improves neural adaptability to stress
• ·Neuroprotection — particularly relevant for patients with cardiovascular risk factors (ischaemia risk)
• ·Mood — dopaminergic and serotonergic modulation
• ·Often paired with Selank (Selank for anxiety/cortisol; Semax for cognition/BDNF)

Semax is a registered pharmaceutical in Russia and has been studied in clinical settings for stroke recovery, cognitive enhancement, and anxiety. Its BDNF mechanism is consistent with an established body of neuroscience research. Intranasal delivery provides efficient CNS access.

Intranasal administration, 200–600 mcg per day. Physician determines dose based on cognitive symptom profile and cortisol markers. Often cycled — 2 weeks on, 2 weeks off.

DSIP (Delta Sleep-Inducing Peptide) is a neuropeptide first isolated from rabbit cerebral venous blood in 1974. It promotes delta-wave (deep, slow-wave) sleep by modulating the HPA axis — specifically by reducing corticotropin-releasing hormone (CRH) activity and normalising the cortisol:melatonin rhythm. Unlike sedative sleep aids (benzodiazepines, z-drugs), DSIP does not suppress REM sleep or create dependence. It addresses the upstream neuroendocrine driver of poor sleep rather than forcing sedation.

• ·Deep (delta-wave) sleep — the phase most critical for GH release, immune function, and metabolic repair
• ·Cortisol rhythm normalisation — elevated AM cortisol and disrupted diurnal cortisol pattern are primary drivers of poor sleep quality
• ·HPA axis dysregulation — the underlying system driving both cortisol excess and sleep disruption
• ·GH secretion — GH is released primarily during delta sleep; restoring sleep architecture amplifies CJC-1295 + Ipamorelin effects
• ·Stress-related insomnia — without dependence or next-day cognitive impairment

DSIP was identified and studied extensively in the 1970s and 1980s, with a solid body of research on its sleep-promoting and HPA-modulatory effects. It is mechanistically distinct from any class of sedative, with no abuse potential and no suppression of restorative sleep stages.

Subcutaneous injection, 100–200 mcg before sleep. Often prescribed alongside CJC-1295 + Ipamorelin as a sleep architecture optimisation stack. Physician determines need based on cortisol, DHEA-S, and testosterone markers.

Epitalon is a synthetic tetrapeptide (Ala-Glu-Asp-Gly) developed by the St. Petersburg Institute of Bioregulation and Gerontology. It is the most studied peptide in the longevity category. Its primary mechanism is activation of telomerase — the enzyme that rebuilds telomere length in somatic cells. Telomere shortening is a primary hallmark of biological aging; Epitalon is the only clinically studied compound that demonstrably activates telomerase in human cells in vitro and in vivo. It also regulates melatonin production through the pineal gland, normalises circadian rhythm, and has demonstrated anti-tumour activity in animal research.

• ·Biological age reduction — the primary longevity application
• ·Telomere length maintenance — addresses a root mechanism of cellular aging
• ·Melatonin regulation — pineal gland normalisation improves sleep quality and circadian function
• ·Immune function — consistent finding across Epitalon research is immune system support in older patients
• ·Hormonal balance — pineal regulation has downstream effects on sex hormones and cortisol
• ·Antioxidant activity — reduction in oxidative stress markers

Epitalon has the most extensive human research base of any peptide in the longevity category. Studies by Professor Vladimir Khavinson and colleagues at the St. Petersburg Institute span 40+ years and include human trials demonstrating increased telomerase activity, telomere elongation in somatic cells, and improved immune function in elderly subjects. It is a registered pharmaceutical in Russia.

Subcutaneous injection, typically used in courses: 10 days on, followed by 3–6 months off. Physician determines course timing based on biological age data and retesting protocol.

GHK-Cu (Glycyl-L-Histidyl-L-Lysine-Copper) is a naturally occurring human peptide that declines dramatically with age — abundant at age 20 (~200 ng/mL plasma), nearly absent by 60 (~80 ng/mL). It acts as a biological signal for tissue repair, activating over 4,000 human genes according to genome analysis — primarily genes involved in tissue remodelling, anti-inflammatory signalling, and antioxidant defence. Injectable GHK-Cu produces systemic effects: collagen synthesis, wound healing acceleration, nerve regeneration, and lung and gut tissue repair. Topical GHK-Cu is available as WellSpry Skin for localised skin applications — the injectable version requires a physician prescription for systemic use.

• ·Systemic tissue repair — skin, gut lining, lung tissue, nerve tissue
• ·Collagen synthesis — relevant for both skin quality and joint integrity during rapid weight loss
• ·Anti-inflammatory gene activation — downstream effect of tissue repair signalling
• ·Wound healing
• ·Nerve regeneration — preliminary data in peripheral neuropathy contexts
• ·Skin quality during rapid GLP-1-driven weight loss (loose skin risk with fast fat loss)

GHK-Cu research spans 50 years, beginning with Loren Pickart's work in the 1970s. It is one of the most extensively studied peptides in skin biology and wound healing. Genome analysis by Pickart and colleagues identified over 4,000 genes modulated by GHK-Cu, making it one of the broadest-acting endogenous peptides identified to date.

Subcutaneous injection, 1–3x per week. Physician determines frequency and duration based on fat loss rate, tissue repair indication, and patient profile.

Kisspeptin is a neuropeptide produced in the hypothalamus that serves as the primary upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis. It stimulates GnRH (gonadotropin-releasing hormone) release, which in turn drives LH (luteinising hormone) and FSH (follicle-stimulating hormone) — the signals that trigger testosterone production in men and oestrogen/progesterone cycling in women. Kisspeptin-10 is the biologically active decapeptide fragment. It addresses hormonal decline at the upstream regulatory level rather than through direct hormone replacement.

• ·LH and FSH normalisation — particularly in patients with central (hypothalamic) rather than gonadal hormone deficiency
• ·Perimenopausal hormonal irregularity — irregular LH/FSH pulsatility is a primary driver of perimenopausal symptoms
• ·Male testosterone support — addresses the upstream signal rather than replacing testosterone directly
• ·Fertility-adjacent hormonal support
• ·Libido — through upstream restoration of the sex hormone cascade
• ·GLP-1 patients: caloric restriction can suppress the HPG axis; Kisspeptin-10 restores the signal

Kisspeptin's role as the master regulator of the HPG axis is established in endocrinology literature. Human studies with kisspeptin-10 and kisspeptin-54 have demonstrated LH pulse stimulation, FSH response, and downstream sex hormone restoration. Research groups at Imperial College London and elsewhere have published extensively on kisspeptin physiology.

Subcutaneous injection, dose and frequency determined by physician based on LH, FSH, testosterone, and oestradiol panel results. Protocol varies significantly between male and female patients and perimenopausal versus premenopausal status.

Thymosin Alpha-1 (Tα1) is an endogenous peptide produced by the thymus gland that declines with age as the thymus involutes. It is a potent immune modulator that enhances dendritic cell maturation, upregulates MHC class II expression, and increases natural killer (NK) cell cytotoxic activity. Unlike non-specific immune stimulants, Tα1 modulates immune function — amplifying response where needed and dampening inappropriate inflammatory activity. It is approved as a pharmaceutical (Zadaxin) in 35+ countries for hepatitis B, hepatitis C, and as an immune adjuvant in oncology.

• ·NK cell function — the immune system's first line against viral infection and cancer surveillance
• ·Chronic viral illness — herpes, EBV reactivation, HPV — where NK function is the relevant immune arm
• ·Immune senescence in older patients — the age-related decline in immune function
• ·Autoimmune modulation — Tα1 has a regulatory rather than purely stimulatory immune effect
• ·Post-illness recovery — immune reconstitution
• ·Employer wellness track: the most defensible clinical immune intervention in the stack

Thymosin Alpha-1 has the most robust clinical evidence base of any peptide in the WellSpry stack. It is FDA-approved as an orphan drug for DiGeorge syndrome and is approved as a pharmaceutical in 35+ countries. Published RCTs exist for hepatitis B, hepatitis C, sepsis, and immune reconstitution post-chemotherapy. Its safety profile is extensively characterised.

Subcutaneous injection, 1.6 mg twice weekly for acute immune support; once weekly for maintenance. Physician determines course length based on immune panel response and clinical presentation.