# CJC-1295 MD — Independent research summaries on a long-acting GHRH analog

> Plain-English overview of CJC-1295 (the DAC-albumin GHRH analog): mechanism, the Teichman 2006 Phase 1 paper, the terminated 2006 Phase 2 program, half-life, and current FDA and WADA status.

A long-acting GHRH analog that couples to serum albumin, raises growth hormone for days, and has a clinical record that begins and ends with a single 2006 Phase 1 paper. Here is what the published literature actually shows.

## The short version

CJC-1295 is a synthetic version of the signal your hypothalamus sends to make your pituitary release growth hormone. The key innovation is a chemical handle — called DAC (Drug Affinity Complex) — that locks the peptide onto a protein already circulating in your blood, keeping it active for days instead of minutes.

What does the science actually show? One solid Phase 1 paper in healthy adults found that a single dose raised growth hormone for at least six days and a downstream signal called IGF-1 for nine to eleven days. The pituitary's own pulsing rhythm stayed intact — the peptide amplified the signal rather than replacing it. Those are the cleanest results on the record.

CJC-1295 is not FDA-approved for any use and never completed Phase 2 trials. It carries real cautions: fluid retention, potential effects on blood sugar, a cancer-risk question from epidemiology, and an FDA immunogenicity flag. If you want to understand what people in research-use communities report — the effects and the downsides — see [the effects page](/effects). Everything cited here traces to primary sources.

## What CJC-1295 is

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH) — the hypothalamic signal that tells the pituitary to release a pulse of growth hormone. The molecule is built from the first 29 amino acids of human GHRH, with four targeted substitutions that protect it from the enzyme DPP-4, plus a small chemical handle on its tail end that lets it lock onto a circulating carrier protein in the blood [1].

That carrier protein is serum albumin — the most abundant protein in human plasma. Once injected under the skin, CJC-1295's tail (a group called maleimide) forms a covalent bond with a single reactive site on albumin (the cysteine at position 34). The resulting peptide-albumin conjugate is what extends the molecule's life in the bloodstream from minutes to days [1][2].

This is the version the literature usually calls CJC-1295 with DAC (Drug Affinity Complex). A second product is sold in research-chemical channels as 'CJC-1295 without DAC' — chemically, that is the same four-substitution backbone without the albumin-binding handle, and its half-life is about thirty minutes rather than several days. The two are often conflated; they are not the same drug in any pharmacologically meaningful sense.

## What the published research actually shows

The human evidence base for CJC-1295 is unusually narrow. One Phase 1 paper (Teichman 2006) gave single subcutaneous doses of 30 to 250 μg/kg to healthy adults and saw growth hormone rise two- to ten-fold for at least six days, with downstream IGF-1 rising 1.5- to 3-fold for nine to eleven days [2]. A companion paper analyzed the same cohort's pulse architecture and showed that the trough GH between pulses rose about 7.5-fold while the natural pulsatile rhythm of pituitary release was preserved [3]. A 2009 proteomics paper looked at stored serum samples from the same cohort and identified five plasma proteins whose levels shifted after a single CJC-1295 dose [8].

That is essentially the published clinical record. A Phase 2 trial in HIV-associated visceral adiposity (NCT00267527, n=192) was terminated in October 2006 after a participant died of an acute coronary event independently judged not to be study-drug related; the sponsor did not restart development and primary efficacy endpoints from the trial were never published in the peer-reviewed literature [9]. No Phase 3 trial has ever been conducted. Everything published in the twenty years since has been mechanistic, analytical (anti-doping detection methods), or regulatory.

## Why this site exists

Most of what you can read about CJC-1295 online is forum copy. The actual literature is small, technically interesting, and easier to read than the noise around it suggests — a handful of peer-reviewed papers, a published clinical-trial registry entry with a cardiac safety event in its footnotes, an FDA briefing document, a WADA prohibited-list entry, and a small body of equine anti-doping analytical work that built the detection methods used today.

This site treats that record as a reading list. Each page summarizes one slice of the published evidence in plain English, cites the primary source, and avoids the two failure modes that dominate online writing on this compound: invented dosing protocols on one side, and reflexive prohibition rhetoric on the other. The compound has a real pharmacological identity. It also has a real regulatory record. Both are worth reading carefully.

## What you'll find on these pages

The **/research** page works through the mechanism, the Phase 1 PK paper, the pulsatility substudy, the GHRH-knockout-mouse growth-restoration study, the equine anti-doping methods, and the terminated Phase 2 program in roughly that order [1][2][3][4][5][6][9].

The **/dosage** page covers the doses actually used in published research — not recommendations. The Phase 1 cohorts were dosed at 30, 60, 125, and 250 μg/kg subcutaneously; the GHRH-knockout mice received 2 μg per injection, equivalent to about 80 μg/kg in a 25-gram animal [2][4]. The page also covers DAC versus non-DAC half-life differences and the practical PK implications.

The **/faq** page answers the questions readers actually arrive with — about the DAC/non-DAC distinction, the 503A regulatory status, the WADA prohibition, the ipamorelin pairing rationale, and the difference between CJC-1295 and tesamorelin (the FDA-approved GHRH analog in the same drug class).

The **/references** page lists every primary source used across the site with DOIs and PubMed or PMC URLs.

None of these pages recommend, dispense, or arrange for the compound. The site is editorial — a reading room, not a clinic.

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An editorial digest of peer-reviewed research — not a clinic, not a vendor, not a prescription.
