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NNMT inhibition raises intracellular NAD+ and preserves S-adenosylmethionine availability. Research documents downstream effects on adipocyte energy expenditure, lipolysis pathways, and cellular methylation balance — pathways implicated in metabolic and longevity research.
Data are predominantly preclinical and early-stage; long-term human data remain limited. Dosing parameters for the injectable form are not well established in published research. Often researched within metabolic and cellular-aging contexts.
AICAR mimics AMP and activates AMPK — the cell’s primary energy sensor. Research documents increased glucose uptake, enhanced fatty-acid oxidation, and mitochondrial biogenesis pathway activation, alongside endurance-capacity pathway effects in research models.
Data are predominantly from research models; poor oral bioavailability is noted. Cardiac caution is documented in research literature. See Safety & Interactions for details.
Anastrozole reversibly binds the aromatase enzyme, blocking the conversion of androgens to estrogens and lowering circulating estradiol. The reversible mechanism allows estrogen levels to be titrated within research protocols.
Bone-density and lipid monitoring are emphasized in research, and over-suppression of estrogen carries its own documented risks. See Safety & Interactions.
AOD-9604 is documented to stimulate lipolysis and inhibit lipogenesis through beta-3 adrenergic pathway signalling, without measurable effect on IGF-1 or blood glucose in research models — distinguishing it from full growth hormone.
Generally well-tolerated in research; dosing parameters are not well established in published human data, which remains limited.
ARA-290 is a synthetic 11-amino acid peptide derived from the helix B region of erythropoietin. It selectively activates the innate repair receptor (IRR) — a tissue-protective receptor distinct from the erythropoietin receptor — without triggering red blood cell production. Research documents activation of anti-apoptotic, anti-inflammatory, and tissue repair signalling pathways. Documented in neuropathic pain research, small nerve fibre repair pathway studies, and metabolic tissue research including sarcoidosis-associated neuropathy pathway data.
Reference concentration: 50–200mcg. Often referenced alongside BPC-157 and TB-500 in nerve and tissue repair research combinations.
Bacteriostatic water (BAC water) is sterile water containing 0.9% benzyl alcohol. The benzyl alcohol prevents bacterial growth, allowing a reconstituted vial to be used multiple times over 28–30 days — unlike regular sterile water which must be used immediately. Research literature documents it as the widely referenced reconstitution solution for research-grade peptides.
The volume of BAC water added determines the concentration. Adding 1mL to a 10mg vial yields 10mg/mL (1mg per 0.1mL). Adding 2mL yields 5mg/mL. The Measurement Calculator is available to determine exact application volumes for a target concentration.
BPC-157 is derived from a protective protein found in gastric juice. Research documents it acts on tissue repair pathway mechanisms including tendon-to-bone repair, growth hormone receptor pathway activity, nitric oxide pathway effects, and inflammatory signalling reduction.
Reference concentration: 250–500mcg daily. Often referenced alongside TB-500 in published tissue repair research combinations. Receptor downregulation has not been reported in published research literature to date.
BPC-157 (Research Peptide Compound) in oral tablet form. Research notes the oral route is referenced for gastrointestinal pathway research, gut barrier integrity, and digestive research applications, with systemic tissue repair and inflammatory signalling pathway effects also documented in published studies.
Reference concentration: 1–2 tablets daily. Long-term administration side effect profiles are documented in research literature. Often referenced alongside BPC-157 Injectable in published tissue repair research combinations.
Amylin is a hormone co-secreted with insulin after meals that acts on satiety signalling pathways in the brain. Cagrilintide mimics this satiety signal continuously, with caloric intake reduction noted as an observed effect in research data. Unlike GLP-1 agents, it acts primarily on the hypothalamus and brainstem via a distinct neural pathway. When combined with a GLP-1, research data notes the effect is additive — CagriSema studies document additive metabolic pathway effects in published research.
Reference concentration noted at 0.25mg. Research documents combination with semaglutide in CagriSema trials. Research notes the amylin pathway mechanism acts on satiety signalling centres independent of dietary variables.
CJC-1295 is a synthetic GHRH analogue that acts on the pituitary gland to stimulate growth hormone release and extends the duration of GH pulses. Ipamorelin is a selective GHRP that triggers targeted GH release without significantly raising cortisol or prolactin — noted in research as a distinction from older GHRPs like GHRP-6. Together they produce synergistic GH amplification: CJC-1295 widens the GH pulse window while Ipamorelin provides the trigger, with GH output pathway data documented in published research. Research notes the liver converts this GH into IGF-1, with adipose metabolism, muscle protein synthesis, tissue repair, and cellular repair pathway effects documented across research periods.
Reference concentration: 100mcg of each peptide (CJC-1295 + Ipamorelin) per application,. Food intake timing pathway interactions are documented in published research literature. Often referenced alongside BPC-157, TB-500, or Tesamorelin in published research combinations.
A collagen-infused topical research compound. Research notes collagen peptides applied topically act on skin barrier pathway function, moisture retention pathway effects, and fine line pathway data. Often referenced alongside systemic peptides such as GHK-Cu, NAD+, and Glutathione in published research combinations.
Often referenced as the topical component of The Fountain, The Bloom, and The Flawless research combinations.
Eloralintide activates amylin receptors in the hindbrain, promoting satiety and slowing gastric emptying through a pathway separate from GLP-1. Research documents complementary glucose-regulation effects, and it is frequently studied alongside GLP-1 agonists.
An investigational amylin analogue; human data are emerging. Often researched in combination with GLP-1 agonists for additive satiety-pathway effects.
As a steroidal “suicide” inhibitor, exemestane permanently inactivates the aromatase enzyme; restoration of activity requires synthesis of new enzyme. Research documents durable estradiol suppression and a mild androgenic profile relative to non-steroidal inhibitors.
Bone-density and lipid monitoring are noted in research. See Safety & Interactions.
GHK-Cu acts on a broad array of regenerative genes — research documents collagen, elastin, and glycosaminoglycan synthesis pathway effects. Research notes wound healing pathway activity, inflammatory signalling reduction, scar tissue remodelling, hair follicle pathway effects, and antioxidant pathway data. Research documents activation of over 4,000 genes associated with cellular restoration and longevity. Endogenous levels are documented to drop approximately 50% between ages 20 and 60 in published research.
Reference concentration noted at 1mg daily. A 30-day washout period between research cycles is documented in published research literature. Often referenced alongside BPC-157 and TB-500 in published research combinations.
Glow is referenced in research for dermal matrix, hair follicle, cellular aging, tissue repair, and inflammatory pathway studies. The BPC-157 + TB-500 combination is a peptide tissue repair combination with documented published research data, with GHK-Cu adding regenerative gene expression and dermal pathway data.
Klow builds on Glow by adding KPV, with published research referencing gut pathway, inflammatory signalling, and immune modulation pathway data. The four-peptide combination provides a comprehensive inflammatory signalling and tissue repair research profile.
Reference concentration: 15 units daily.
Glutathione is a tripeptide (glycine, cysteine, glutamate) produced by every cell in the body. Research notes it neutralizes free radicals, supports liver detoxification, regenerates vitamins C and E, and regulates melanin production. Research notes subcutaneous administration is documented to deliver higher bioavailability compared to oral administration in published studies.
Reference concentration: 600–1500mg, 3–5 times weekly. Research notes Vitamin C is frequently co-referenced for absorption pathway and glutathione regeneration effects. Consistent administration over 4–8 weeks is the documented research period in published melanin regulation pathway studies.
HCG binds to the same receptor as LH, acting on Leydig cells and gonadal tissue to stimulate sex hormone production. In male research subjects on hormonal research compounds, research notes it acts on testicular function and intratesticular testosterone pathways relevant to fertility research. Research notes testosterone pathway effects in male subjects with secondary hypogonadism when used as a standalone compound. In female research subjects, research notes progesterone production and ovulation pathway effects.
Reference concentration: 250–500IU 2–3 times per week.
Lipo-C is a combination of lipotropic agents that act on fat metabolism in the liver. Research notes methionine acts on fat deposit breakdown pathways. Inositol is documented to act on fat redistribution and cholesterol pathway activity. Choline is noted to act on hepatic fat accumulation pathways and fat transport mechanisms. Combined with B12 and B-complex vitamins, cellular energy production pathway effects and metabolic clearance mechanisms are noted as observed effects.
Reference concentration: 25–54mg (25 units) 2–3 times per week,. No washout period required. Often referenced alongside semaglutide, tirzepatide, or other metabolic research combinations as a complementary compound.
Melanotan 2 activates melanocortin receptors — MC1R drives melanin synthesis (pigmentation), while MC4R modulates central libido and appetite pathways. This non-selective activation underlies both its pigmentary and central effects in research.
Skin and mole monitoring are emphasized in research given MC1R melanocyte activity. Nausea and spontaneous erections are commonly documented. See Safety & Interactions.
MOTS-C is produced by mitochondria under metabolic stress and travels to the nucleus to regulate gene expression. Research notes it activates AMPK (a key metabolic regulator), with glucose uptake in muscle, adipose reduction, and mitochondrial efficiency pathway effects documented. Studies document physical endurance pathway data, obesity-related inflammatory signalling reduction, and age-related metabolic pathway changes — including in the absence of diet or exercise modifications.
Reference concentration: 1mg daily for 5 days per week, or 5mg 2–3 times per week. Escalation up to 10–15mg per research application in performance-focused research. Often referenced alongside NAD+, Somatropin, and Tesamorelin in comprehensive metabolic and cellular aging research combinations.
NAD+ is a coenzyme present in every living cell, essential for converting food into cellular energy (ATP), repairing damaged DNA, regulating circadian rhythm, and controlling inflammatory signalling. Research notes it activates sirtuins and PARPs — proteins that protect DNA integrity and are associated with biological aging pathways. Research notes subcutaneous administration is documented to deliver higher bioavailability compared to oral administration in published studies.
Reference concentration noted at 25–50mg daily increasing up to 100mg+. A mild flushing sensation during application is commonly noted in research and slow application rate is noted to reduce this. Often referenced alongside MOTS-C for mitochondrial pathway research. Particularly documented in research involving cellular energy, cognitive pathway, and age-related metabolic pathway studies.
Both deliver the same NAD+ molecule and produce the same cellular pathway activity. The distinction is entirely in the documented application experience in research subject data.
PT-141 activates MC4R within the central nervous system to modulate sexual-arousal pathways — a central mechanism distinct from the vascular, blood-flow-based action of PDE5 inhibitors. This allows activity independent of the vascular pathway in research.
Transient blood-pressure elevation and nausea are documented in research. Its central mechanism does not depend on the vascular pathway. See Safety & Interactions.
Retatrutide activates three hormone receptors simultaneously. Research notes GLP-1 activation is associated with reduced appetite signalling and slowed digestion. GIP activation is associated with enhanced insulin response and fat metabolism pathway effects. Glucagon activation is documented to increase metabolic rate and act on fat mobilisation pathways — including visceral and hepatic fat. Phase 2 trials documented 24% body weight reduction observed over 48 weeks in published research — as documented in published Phase 2 research data.
Reference concentration noted at 2.5mg. GI side effects are noted in early research data — research documents these as resolving in the majority of research subjects. Glucagon activation is noted in research as associated with heart rate pathway activity. Research notes combination with other GLP-1 agents is not documented in published research combinations.
Revive+ combines NAD+ (a cofactor in cellular energy and DNA-repair pathways), MOTS-C (a mitochondrial-derived metabolic regulator), and 5-Amino-1MQ (NNMT inhibition supporting NAD+ salvage). Together these target cellular energy, mitochondrial function, and metabolic-flexibility pathways.
A combination product — see the individual NAD+, MOTS-C, and 5-Amino-1MQ entries for full mechanism detail. Effects of rapid NAD+ administration are noted in research. See Safety & Interactions.
Selank is a synthetic analogue of the endogenous immunomodulatory peptide tuftsin. Research notes it modulates GABA pathway activity, increases BDNF expression, and acts on serotonin and dopamine pathway signalling. Documented for anxiolytic pathway effects without the sedative or dependency pathway effects observed with conventional anxiolytic compounds. Research additionally notes immunomodulatory pathway activity and memory consolidation pathway data.
Reference concentration: 100–500mcg. Often referenced alongside Semax in published research for complementary nootropic and anxiolytic pathway research combinations.
Semaglutide is a GLP-1 receptor agonist that mimics the natural hormone GLP-1, released after eating. It slows digestion, increases satiety signalling, reduces appetite signals from the brain, and acts on blood sugar regulation pathways. Research notes it targets both gut hormone pathways and the brain's reward centre, with food reward signalling pathway effects documented in research data.
Reference concentration noted at 0.25mg. Nausea is documented in research as resolving in the majority of research subjects within 2–4 weeks of each concentration increase. Research notes consistent weekly timing regardless of meals. Outcomes are documented alongside dietary and lifestyle variables in published studies.
Semax is a synthetic analogue of ACTH (adrenocorticotropic hormone). Research notes it increases BDNF (brain-derived neurotrophic factor), acts on dopamine and serotonin pathway activity, and is documented for neuroprotective pathway effects. Documented in Russian pharmaceutical research for cognitive disorders, neurological research, and ADHD pathway studies. Cognitive pathway, focus, and mood pathway effects among observed data points.
Reference concentration: 100–300mcg. Often referenced alongside BPC-157 for neuroprotective pathway research and NAD+ for comprehensive cognitive pathway research combinations.
Research documents Sildenafil as acting by blocking PDE5 to increase nitric oxide activity and vasodilation pathway effects. Clinical data notes an extensively documented side effect profile. Food is noted in research to slow absorption. It is referenced for acute on-demand administration patterns, compared to Tadalafil's longer-acting profile.
Research reference: 250mg with onset noted at approximately 1 hour in research data. Food noted to slow absorption. Combination with nitrates documented as contraindicated in clinical literature. Headache and flushing are noted side effects in clinical data.
SLU-PP-332 is a novel exercise mimetic compound that activates ERR (estrogen-related receptor) pathways — the same pathways activated by endurance exercise. Research data documents fat oxidation, endurance, metabolic rate, and cardiovascular pathway effects as observed data points.
Reference concentration noted at 1 tablet daily in research data. Often noted in combination with other metabolic research agents. For research and educational purposes only.
Research documents Human Growth Hormone as having extensive anabolic pathway effects. Research notes it acts on IGF-1 production, lipolysis pathways, muscle protein synthesis, collagen production, and immune function pathways. Somatropin levels are documented to decline with age in published research — with wide-ranging pathway effects on body composition, skin, joints, sleep, and energy documented across research periods.
Reference concentration: 2IU daily.
SS-31 (Elamipretide) is a mitochondria-targeted antioxidant peptide. It selectively concentrates in the inner mitochondrial membrane where it binds cardiolipin — a phospholipid critical for maintaining membrane integrity and electron transport chain function. Research documents reduction in reactive oxygen species (ROS) production, preservation of mitochondrial membrane potential, and ATP synthesis pathway support. Documented in cardiac, renal, and neurological tissue research for cytoprotective pathway effects under oxidative stress conditions.
Reference concentration: 2–10mg. Often referenced alongside NAD+ and MOTS-C for comprehensive mitochondrial and cellular energy pathway research combinations.
Research documents Tadalafil as acting by blocking PDE5 to increase nitric oxide activity and vasodilation pathway effects. Clinical data notes an extensively documented side effect profile. Unlike shorter-acting PDE5 compounds, research documents that food does not meaningfully affect absorption. Its extended half-life is referenced in research for both on-demand and lower-concentration daily administration patterns, compared to Sildenafil's acute on-demand profile.
Research reference: extended-duration parameter documented up to approximately 36 hours in research data. Food noted in research as not meaningfully affecting absorption. Combination with nitrates documented as contraindicated in clinical literature. Headache, flushing, and back pain are noted side effects in clinical data.
TB-500 is a synthetic version of Thymosin Beta-4, a protein found throughout the body with a documented role in tissue repair pathway activity. Research notes it works systemically — proximity to the area of interest for administration is not required. TB-500 acts on actin upregulation (critical for cell movement), angiogenesis pathway activity, and inflammatory signalling reduction, with tendon, muscle, ligament, and cardiac tissue repair pathway effects documented in research.
Reference concentration: 2.5mg. Often referenced alongside BPC-157 in published research combinations.
Tesamorelin acts on the pituitary gland to release growth hormone in a natural, pulsatile manner. Research notes elevated GH signals the liver to produce IGF-1, with adipose metabolism, muscle protein synthesis, and tissue repair pathway effects documented in research. Research-documented for visceral adipose reduction and noted in research for cellular repair, body composition, and metabolic pathway data.
Reference concentration: 1.4–2mg daily. Often referenced alongside BPC-157 or GHK-Cu in published research combinations.
Tesofensine is a triple monoamine reuptake inhibitor originally developed for neurological conditions and later studied for metabolic pathway effects. Research documents its mechanism as blocking the reuptake of dopamine, serotonin, and norepinephrine — with appetite signalling pathway reduction and increased resting energy expenditure noted as observed effects in research data.
Reference concentration: 0.25–0.5mg daily. Can be referenced in combination with GLP-1 compounds. Extended research period pathway response data is documented in published research literature.
The cypionate ester extends testosterone’s half-life for sustained release. Testosterone binds androgen receptors and influences muscle and bone pathways, erythropoiesis, libido, and mood — the pathways documented across androgen research.
Clinical protocols vary. Hematocrit, prostate, estradiol, and lipid monitoring are emphasized in research. See Safety & Interactions for the full profile.
Retatrutide is a triple receptor agonist activating GLP-1, GIP, and glucagon simultaneously, with fat mobilisation and appetite signalling pathway effects documented in published data. Tirzepatide adds synergistic GIP/GLP-1 dual action, with compounding appetite signalling and metabolic pathway data documented in research. Administration parameters for combination use are documented in published research data. Tesofensine works through an entirely different mechanism, acting on the reuptake of dopamine, norepinephrine, and serotonin in the brain, with CNS hunger signalling and energy expenditure pathway effects documented in research. Together these three compounds act on adipose pathways from three separate biological mechanisms simultaneously, with research data documenting compounding metabolic effects across published research.
Administration parameters and combination use references for this research combination are documented in published research data.
Tirzepatide mimics two naturally occurring gut hormones — GIP and GLP-1. Together they slow gastric emptying, reduce appetite signalling, act on blood sugar regulation pathways, and act on the brain's satiety centres. Research data documents metabolic pathway effects in comparative trials with semaglutide.
Reference concentration of 2.5mg. Escalation parameters are documented in published clinical literature. Nausea and mild GI effects in the first few weeks are commonly noted in research and documented as resolving in the majority of research subjects. Administration parameters are documented in published clinical literature.
The Trinity combines three complementary research compounds. TB-500 (Thymosin Beta-4) acts systemically on actin upregulation, angiogenesis pathway activity, and inflammatory signalling reduction. BPC-157 (Body Protection Compound-157) supports tendon, ligament, gut lining, and connective tissue repair pathways through growth factor signalling and angiogenesis. KPV (Lys-Pro-Val) is a tripeptide documented for anti-inflammatory pathway activity, particularly within intestinal tissue and wound repair research contexts. Together the three compounds address overlapping but distinct repair and signalling pathways.
Reference concentration parameters are documented in published research literature for each individual compound. The Trinity is referenced as a comprehensive repair and recovery research combination. Often referenced alongside NAD+ for cellular energy pathway support during tissue repair research protocols.
The Wolverine combines TB-500 and BPC-157 — two peptides with complementary tissue repair mechanisms. Research documents TB-500 as acting on systemic tissue repair through cell migration and angiogenesis pathways. Research documents BPC-157 as acting on local tendon, ligament, muscle, and gut tissue repair pathways while reducing inflammatory signalling. Together research documents comprehensive pathway coverage — systemic and local, structural and vascular.
Pre-blended vial — each reference contains both compounds at equal ratio. Three reference tiers noted in research: Tier 1 Reference (general maintenance research): 2.5mg blend · 2x weekly · 4–6 weeks. Tier 2 Reference (active tissue repair research): 5mg blend · 2x weekly · 4–6 weeks, then 2.5mg once weekly. Tier 3 Reference (intensive research): 5mg blend · daily for first 2 weeks, then 5mg · 2–3x weekly for weeks 3–6. Both compounds are present in each administration.
| Concentration | Units |
|---|---|
| 54mg | 25 |
| 108mg | 50 |
| 162mg | 75 |
| 216mg | 100 |
| Dose | Units |
|---|---|
| 50mg | 20 |
| 100mg | 40 |
| 250mg | 100 |
| 500mg | 200 |
| Concentration | Units |
|---|---|
| 1mg | 6 |
| 2mg | 12 |
| 3mg | 18 |
| Concentration | Units |
|---|---|
| 1mg | 3 |
| 2mg | 6 |
| 3mg | 9 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 25 |
| Week 3–4 | 5mg | 50 |
| Week 5–8 | 7.5mg | 75 |
| Week 9–12 | 10mg | 100 |
| Week 13–16 | 12.5mg | 125 |
| Week 17+ | 15mg | 150 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 19 |
| Week 3–4 | 5mg | 38 |
| Week 5–8 | 7.5mg | 56 |
| Week 9–12 | 10mg | 75 |
| Week 13–16 | 12.5mg | 94 |
| Week 17+ | 15mg | 113 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 15 |
| Week 3–4 | 5mg | 30 |
| Week 5–8 | 7.5mg | 45 |
| Week 9–12 | 10mg | 60 |
| Week 13–16 | 12.5mg | 75 |
| Week 17+ | 15mg | 90 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 13 |
| Week 3–4 | 5mg | 25 |
| Week 5–8 | 7.5mg | 38 |
| Week 9–12 | 10mg | 50 |
| Week 13–16 | 12.5mg | 63 |
| Week 17+ | 15mg | 75 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 8 |
| Week 3–4 | 5mg | 15 |
| Week 5–8 | 7.5mg | 22 |
| Week 9–12 | 10mg | 30 |
| Week 13–16 | 12.5mg | 38 |
| Week 17+ | 15mg | 45 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 6 |
| Week 3–4 | 5mg | 12 |
| Week 5–8 | 7.5mg | 18 |
| Week 9–12 | 10mg | 24 |
| Week 13–16 | 12.5mg | 30 |
| Week 17+ | 15mg | 36 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 5 |
| Week 3–4 | 5mg | 11 |
| Week 5–8 | 7.5mg | 16 |
| Week 9–12 | 10mg | 21 |
| Week 13–16 | 12.5mg | 27 |
| Week 17+ | 15mg | 32 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 0.25mg | 3 |
| Week 3–4 | 0.5mg | 5 |
| Week 5–8 | 1mg | 10 |
| Week 9–12 | 1.7mg | 17 |
| Week 17+ | 2.4mg | 24 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 0.25mg | 3 |
| Week 3–4 | 0.5mg | 5 |
| Week 5–8 | 1mg | 10 |
| Week 9–12 | 1.7mg | 17 |
| Week 17+ | 2.4mg | 24 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 0.25mg | 3 |
| Week 3–4 | 0.5mg | 5 |
| Week 5–8 | 1mg | 10 |
| Week 9–12 | 1.7mg | 17 |
| Week 17+ | 2.4mg | 24 |
| Concentration | Units |
|---|---|
| 1mg | 10 |
| 2mg | 20 |
| Concentration | Units |
|---|---|
| 1mg | 10 |
| 2mg | 20 |
| Concentration | Units |
|---|---|
| 250mcg | 5 |
| 500mcg | 10 |
| 1mg | 20 |
| 1.7mg | 34 |
| 2.4mg | 48 |
| Concentration | Units |
|---|---|
| 250mcg | 2.5 |
| 500mcg | 5 |
| 1mg | 10 |
| 1.7mg | 17 |
| 2.4mg | 24 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 25 |
| Week 3–4 | 5mg | 50 |
| Week 5–8 | 7.5mg | 75 |
| Week 9–12 | 10mg | 100 |
| Week 13–16 | 12.5mg | — |
| Week 17+ | 15mg | — |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 19 |
| Week 3–4 | 5mg | 38 |
| Week 5–8 | 7.5mg | 56 |
| Week 9–12 | 10mg | 75 |
| Week 13–16 | 12.5mg | 94 |
| Week 17+ | 15mg | 113 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 15 |
| Week 3–4 | 5mg | 30 |
| Week 5–8 | 7.5mg | 45 |
| Week 9–12 | 10mg | 60 |
| Week 13–16 | 12.5mg | 75 |
| Week 17+ | 15mg | 90 |
| Week | Concentration | Units |
|---|---|---|
| Week 1–2 | 2.5mg | 13 |
| Week 3–4 | 5mg | 25 |
| Week 5–8 | 7.5mg | 38 |
| Week 9–12 | 10mg | 50 |
| Week 13–16 | 12.5mg | 63 |
| Week 17+ | 15mg | 75 |
| Concentration | Units |
|---|---|
| 1IU | 6 |
| 2IU | 12 |
| 3IU | 18 |
| 4IU | 24 |
| 5IU | 30 |
| 6IU | 36 |
| Concentration | Units |
|---|---|
| 1IU | 5.5 |
| 2IU | 11 |
| 3IU | 16.5 |
| 4IU | 22 |
| 5IU | 27.5 |
| 6IU | 33 |
| Concentration | Units |
|---|---|
| 500IU | 20 |
| 1500IU | 60 |
| 2500IU | 100 |
| Concentration | Units |
|---|---|
| 500IU | 15 |
| 1500IU | 45 |
| 2500IU | 75 |
| Concentration | Units |
|---|---|
| 25mg | 20 |
| 50mg | 40 |
| 75mg | 60 |
| 100mg | 80 |
| Concentration | Units |
|---|---|
| 25mg | 15 |
| 50mg | 30 |
| 75mg | 45 |
| 100mg | 60 |
| Concentration | Units |
|---|---|
| 25mg | 10 |
| 50mg | 20 |
| 75mg | 30 |
| 100mg | 40 |
| Concentration | Units |
|---|---|
| 1mg | 7 |
| 2mg | 15 |
| 3mg | 22 |
| 4mg | 30 |
| 5mg | 37 |
| Concentration | Units (mL) |
|---|---|
| 100mg | 27 |
| 200mg | 53 |
| 300mg | 80 |
| 400mg | 107 |
| 600mg | 160 |
| Total Dose | Units |
|---|---|
| 2.33mg | 10 |
| Total Dose | Units |
|---|---|
| 2.67mg | 10 |
| 4mg | 15 |
| 5.33mg | 20 |
| Total Dose | Units |
|---|---|
| 300mcg | 3 |
| 500mcg | 5 |
| 600mcg | 6 |
| 700mcg | 7 |
| Protocol | Total Dose | Units |
|---|---|---|
| Protocol 1 | 500mcg | 5 |
| Protocol 2 | 1mg | 10 |
| Concentration | Units |
|---|---|
| 2.5mg | 15 |
| 5mg | 30 |
| 10mg | 60 |
| Concentration | Units |
|---|---|
| 1mg | 10 |
| 2mg | 20 |
| 4mg | 40 |
| Total Dose | Units |
|---|---|
| 0.75mg | 7.5 |
| 1.05mg | 10.5 |
| 1.5mg | 15 |
| Concentration | Units |
|---|---|
| 250mcg | 2.5 |
| 500mcg | 5 |
| Concentration | Units |
|---|---|
| 300mcg | 3 |
| 500mcg | 5 |
| 700mcg | 7 |
| 1mg | 10 |
| Concentration | Units |
|---|---|
| 300mcg | 3 |
| 500mcg | 5 |
| 700mcg | 7 |
| 1mg | 10 |
| Concentration | Units |
|---|---|
| 1mg | 7 |
| 3mg | 20 |
| 6mg | 40 |
| 9mg | 60 |
| Concentration | Units |
|---|---|
| 300mcg | 3 |
| 500mcg | 5 |
| 750mcg | 7.5 |
| 1mg | 10 |
| Concentration | Units |
|---|---|
| 300mcg | 3 |
| 500mcg | 5 |
| 750mcg | 7.5 |
| 1mg | 10 |
| Concentration | Units |
|---|---|
| 500mcg | 5 |
| 1mg | 10 |
| 2mg | 20 |
| Concentration | Units |
|---|---|
| 500mcg | 5 |
| 1mg | 10 |
| 2mg | 20 |
| Concentration | Units |
|---|---|
| 1mg | 6 |
| 2mg | 12 |
| 3mg | 18 |
| 4mg | 24 |
| 5mg | 30 |
| Dose | Units |
|---|---|
| 1mg | 3 |
| 2mg | 6 |
| 3mg | 9 |
| Concentration | Units |
|---|---|
| 300mcg | 3 |
| 400mcg | 4 |
| 500mcg | 5 |
| Dose | Units |
|---|---|
| 500mcg | 5 |
| 1mg | 10 |
| 2mg | 20 |
| Dose | Units |
|---|---|
| 250mcg | 2.5 |
| 500mcg | 5 |
| 750mcg | 7.5 |
| 1mg | 10 |
| Dose | Units |
|---|---|
| 13mg | 20 |
| 24mg | 40 |
| 36mg | 60 |
| 48mg | 80 |
| 60mg | 100 |
| Total Dose | Units |
|---|---|
| 0.77mg | 4.5 |
| 1.55mg | 9 |
Retatrutide activates GLP-1, GIP, and glucagon receptors with adipose mobilisation pathway effects. Tirzepatide adds dual GLP-1/GIP appetite signalling pathway effects. Tesofensine acts on metabolic rate pathways through CNS mechanisms. The triple-pathway combination produces compounding metabolic effects.
Research documents Retatrutide's triple-receptor activation combined with Cagrilintide's amylin satiety pathway and Tesofensine's metabolic effects as a comprehensively documented metabolic research combination. Research notes Retatrutide activates glucagon receptors — with metabolic rate pathway increases documented in research — while Cagrilintide is documented to act on inter-meal satiety signalling pathways.
Tirzepatide acts on appetite signalling and glucose metabolism pathways. Cagrilintide — an amylin analogue — adds satiety signalling through a completely different pathway, acting on satiety signalling pathway centres independently of GLP-1. Tesofensine acts on metabolic rate pathways through CNS mechanisms. Research notes side effect profile data for this combination.
Research documents this combination as acting on visceral (deep abdominal) adipose tissue through three distinct mechanisms. Tirzepatide is noted in research to act on appetite signalling pathways with caloric intake reduction noted. Tesamorelin — research-documented for visceral adipose reduction — is noted to stimulate GH release with abdominal adipose pathway effects documented in research. Tesofensine acts on overall metabolic rate pathways. Adipose pathway changes and abdominal body composition pathway data are documented in research.
Centred around the Glow Blend — a proprietary formulation noted in research for dermal pathway effects, hydration, and melanin regulation pathway data. Combined with NAD+ for cellular energy pathway activity and Glutathione for systemic oxidative stress pathway effects and melanin regulation. The Collagen Complex is a topical peptide research compound included in this combination. Observed pathway effects from the early weeks of the research period.
The Klow Blend at 80mg is a higher-concentration proprietary formula noted in research for dermal matrix pathway effects, collagen synthesis pathway data, and cellular repair pathway activity. Combined with NAD+ and Glutathione for full systemic cellular research coverage. The Collagen Complex is a topical peptide research compound included in this combination.
Research documents GHK-Cu as acting on collagen synthesis, dermal matrix pathway effects, and skin repair pathway data at the cellular level. NAD+ is noted in research to act on mitochondrial energy and DNA repair pathways. Glutathione acts on melanin regulation, oxidative stress pathways, and systemic antioxidant mechanisms. The Collagen Complex is a topical peptide research compound included in this combination.
| Phase / Day(s) | Dose & Frequency |
|---|---|
| Days 1–2 (Ramp) | 2.5 mg once daily |
| Days 3+ (Standard) | 5 mg once daily |
| Phase / Week(s) | Dose & Frequency |
|---|---|
| Weeks 1–2 | 1 mg (1× daily) |
| Weeks 3–4 | 2 mg (1× daily) |
| Weeks 5–8 | 3 mg (1× daily) |
| Phase / Week(s) | Dose & Frequency |
|---|---|
| Weeks 1–4 | 300 mcg (1× daily) |
| Weeks 5–12 | 400–500 mcg (1× daily) |
| Phase / Week(s) | Dose & Frequency |
|---|---|
| Week 1 | 1 mg (1× daily) |
| Week 2 | 2 mg (1× daily) |
| Weeks 3–4 | 4 mg (1× daily) |
| Phase / Week(s) | Dose & Frequency |
|---|---|
| Weeks 1–4 | 300 mcg (1× daily) |
| Weeks 5–8 | 500 mcg (1× daily) |
| Phase / Week(s) | Dose & Frequency |
|---|---|
| Weeks 1–4 | 500 mcg (2× daily) |
| Weeks 5–8 | 750 mcg (2× daily) |
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