⟁ V-Series Protocol
Natural GH-pathway optimization, without exogenous GH risks
Every component is individually sourced, third-party verified, and dispensed within physician supervision. Tap any compound for its full clinical reference.
A conservative two-compound protocol for patients pursuing physician-supervised optimization of the growth hormone axis. Pairs a GHRH analogue with a selective ghrelin-receptor agonist to amplify the body's own pulsatile GH release - without exogenous GH administration. The protocol is administered as a daily subcutaneous injection, typically pre-sleep on an empty stomach, to align with the body's natural overnight GH pulse. Used for body-composition support, recovery from training load, and IGF-1 trend management in healthy adults under clinical supervision.
CLINICAL INDICATION: Healthy adults pursuing physician-supervised body-composition or recovery optimization; not for diagnosed GH deficiency (different therapy class) and not for muscle-mass claims outside supervised clinical context
CJC-1295 (No DAC) extends the GHRH-receptor signal; Ipamorelin acts through the ghrelin/GHS-R pathway with minimal cortisol or prolactin effect. The two pathways converge on amplified endogenous GH pulses, measured downstream by IGF-1. The stack does not introduce exogenous GH; it modulates the body's own secretion pattern.
A deliberately conservative GH-axis stack: two compounds, complementary mechanisms, no redundancy. Designed for patients who want measurable IGF-1 optimization with the cleanest possible monitoring picture - not a multi-compound protocol whose individual contributions cannot be disentangled.
A note for patients already on a SERM (e.g. enclomiphene or clomiphene): SERMs can modestly lower IGF-1 - recent data found reduced IGF-1 in most treated men (Mogar et al., J Endocr Soc 2025) - so some patients on SERM therapy consider a GH-axis stack like this one to offset that dip. If this applies to you, it is a monitoring consideration to raise with your physician, not a self-directed protocol: Vivre does not supply enclomiphene, and whether the two are appropriate together (and at what point IGF-1 is read) is a clinical decision. Your IGF-1 here would be interpreted against the SERM rather than in isolation.
| What's in the box | Specification | Per month |
|---|---|---|
| CJC+IPA Blend (CJC-1295 No DAC 5mg + Ipamorelin 5mg) | 10mg total per vial · approximately 3 vials in this order for typical daily protocols | 3× |
GHRH / GHRP secretagogues - Tesamorelin, CJC-1295, Ipamorelin, V-G1
These protocols gently restore your body’s own pulsing release of growth hormone rather than replacing it. Because growth hormone also affects blood sugar, monitoring confirms two things: that it is working, and that it is doing so safely.
Incremental approach. Vivre starts below the standard dose and advances only on tolerance. This monitoring is the safety scaffold for that conservative approach.
Educational only - not medical advice or a dosing instruction. Your physician orders the tests, sets your dose, interprets results, and decides if a protocol is right for you. See the Informed Consent & Disclaimer for full terms.
| Biomarker | Why It's Monitored | Baseline | Cadence |
|---|---|---|---|
| IGF-1 | Primary efficacy marker - direct downstream readout of GH-axis amplification | Yes | Wk 6, 12 |
| IGFBP-3 | IGF-1 binding-protein context; bioavailable-IGF interpretation | Yes | Wk 6, 12 |
| Fasting glucose | Primary safety marker - GH-axis activity can affect glucose handling | Yes | Wk 6, 12 |
| HbA1c | Longer-term glycaemic safety surveillance | Yes | Baseline + wk 12 |
| Fasting insulin | Insulin-sensitivity trend during GH-axis modulation | Yes | Wk 6, 12 |
| Thyroid panel (TSH, fT4) | GH-axis activity can interact with thyroid function | Yes | Baseline + wk 12 |
| Lipid panel | Cardiometabolic surveillance | Yes | Baseline + wk 12 |
| Cortisol (AM) | Ipamorelin is selective for GH release with minimal cortisol effect; confirmed at baseline | Baseline only | Re-check if clinically indicated |
| Prolactin | Same selectivity confirmation (minimal prolactin effect) | Baseline only | Re-check if clinically indicated |
| Retinopathy screen (where indicated) | IGF-1 elevation is contraindicated in proliferative retinopathy | Yes | Baseline screen mandatory |
| Malignancy screen (history-based) | Active or recent malignancy is an absolute contraindication | Yes | Baseline screen mandatory |
| Body composition (DEXA where indicated) | Adjunctive composition tracking - not a primary endpoint | Optional | Baseline + wk 12 if indicated |
| Tolerability log | Subjective response (sleep, recovery, injection-site tolerance) | Yes | Ongoing |
Two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults aged 21–61 (DOI 10.1210/jc.2005-1536). A single subcutaneous injection produced dose-dependent increases in mean plasma GH (2–10× for ≥6 days) and IGF-I (1.5–3× for 9–11 days); estimated half-life 5.8–8.1 days. After multiple doses, mean IGF-I stayed above baseline up to 28 days, with evidence of cumulative effect. No serious adverse reactions; well tolerated at 30–60 μg/kg. CRITICAL FRAMING: the studied agent was the DAC-modified long-acting variant, which produces SUSTAINED (continuous) GH/IGF-I elevation. Vivre uses the No-DAC (Mod GRF 1-29) form, which has a ~30-minute half-life and produces PULSATILE GH release that better mimics physiology. This study supports the GH-axis mechanism but does not endorse continuous-elevation (DAC) dosing for longevity use.
View on publisher ↗Foundational preclinical and early clinical study establishing Ipamorelin's selectivity profile. In swine, no GH secretagogue tested affected FSH, LH, PRL, or TSH plasma levels - but GHRP-6 and GHRP-2 elevated ACTH and cortisol meaningfully, while Ipamorelin did not (even at doses 200-fold above the ED50 for GH release). This selectivity is the principal clinical reason Ipamorelin is preferred in modern GH-axis stacks over earlier GHRPs.
View on publisher ↗Preclinical rat study examining downstream skeletal effects of Ipamorelin-driven GH release. Demonstrated dose-dependent increases in longitudinal bone growth via the GH/IGF-1 axis. Important methodology framing: rat model with pre-pubertal skeletal growth - does not translate directly to adult human use, but supports the IGF-1 elevation mechanism that anchors body-composition and recovery applications.
View on publisher ↗| Additional Marker | Why It's Added | Cadence |
|---|---|---|
| Waist circumference / visceral metric | Tesamorelin's primary clinical outcome - central/visceral fat | Baseline + wk 6, 12 |
| Lipid panel (full fractions) | Visceral fat mobilization affects lipid handling | Wk 6, 12 |
| Fasting glucose + HbA1c | Already in V-G1 base; tracked more closely with two GHRH analogues active | More frequent than base - physician set |
| ALT / AST | Hepatic surveillance when visceral fat is mobilizing rapidly | Wk 6, 12 |
| IGF-1 (already in V-G1) | Closer attention - two GHRH analogues + ghrelin agonist will push IGF-1 higher | Same cadence as base, with tighter upper-bound monitoring |
The Audit is complimentary for the Batch 001 cohort. Your physician will review your data, confirm protocol suitability, and initiate the V-G1 allocation if appropriate.
Are you 18 years of age or older?