one name, two drugs

CJC-1295 is the name shared by two related but pharmacologically distinct synthetic peptides built on the GHRH(1-29) backbone. The no-DAC variant, also called modified GRF(1-29), has a roughly 30 minute plasma half-life and is dosed daily. The DAC variant carries a maleimide linker that bolts the peptide onto albumin in vivo, stretching its effective half-life to 6 to 8 days (Teichman et al. 2006; Jetté et al. 2005).

Both variants act upstream at the pituitary GHRH receptor to ask the body to release its own growth hormone. CJC-1295 came out of ConjuChem Biotechnologies in the early 2000s and has a single published Phase I trial in healthy adults plus a halted Phase II trial in HIV-associated lipodystrophy (NCT00267527; AIDSmap 2006). The molecule sits on the FDA 503A Category 2 list for significant safety concerns and is named on the WADA Prohibited List under S2.2 (fda_503a_bulks; WADA 2026).

~30 min vs ~6-8 d

no-DAC vs DAC half-life

1 trial

Phase I PK/PD in healthy adults (Teichman 2006)

503A cat 2

FDA listing for significant safety concerns

WADA S2.2

prohibited in- and out-of-competition

cjc-1295 in plain terms

a 30-residue analog of the front half of natural GHRH, with four amino-acid swaps that protect it from the enzymes that normally chew GHRH apart in minutes.

a synthetic copy of growth hormone-releasing hormone

Natural GHRH is a 44-residue hormone made in the hypothalamus that asks the pituitary for a pulse of growth hormone. Researchers showed in the 1980s that the first 29 residues alone keep almost all of the receptor-activating power. That short fragment is called GHRH(1-29), or sermorelin when supplied as a drug (Mayo 1992).

the four substitutions that define the cjc-1295 backbone

CJC-1295 starts from GHRH(1-29) and changes four residues to fix four different failure modes. D-Ala2 blocks the DPP-IV enzyme that normally inactivates GHRH within minutes. Gln8 replaces an asparagine that tended to deamidate in the vial.

Ala15 replaces a glycine in a way that increases binding affinity at the GHRH receptor. Leu27 replaces a methionine that tended to oxidize and lose activity. Together these four swaps give you the molecule called modified GRF(1-29), which is the same backbone shared by both CJC-1295 variants (Jetté et al. 2005).

the one thing that splits the two variants

CJC-1295 no-DAC stops there. CJC-1295-DAC adds one more piece: a maleimide group on a C-terminal lysine. That single chemical handle is what bolts the peptide onto plasma albumin once it reaches the bloodstream, and it is what turns a daily peptide into a weekly one (Léger et al. 2004; Jetté et al. 2005).

no-dac vs dac: one name, two drugs

the single most important distinction in this whole course. miss this and every dose figure, every half-life, and every protocol you read online will land in the wrong column.

why "cjc-1295" alone is not enough information

When a paper, a vendor, or a forum post says "CJC-1295," you cannot tell from the name alone whether they mean a peptide with a half-life of 30 minutes or one with a half-life of 6 to 8 days. The two variants are roughly 300 times apart on the half-life axis. Their typical research dose ranges differ by about 10 times, and giving one when the other was intended is the most common community safety hazard for this molecule.

no-DAC variant

modified GRF(1-29)

half-life: about 30 minutes in plasma
frequency: typically 1-3 daily SubQ injections in community use
pulsatility: each dose produces one short GH pulse, similar to sermorelin
extra chemistry: none beyond the four backbone substitutions
best mental model: a stabilized sermorelin

DAC variant

CJC-1295-DAC

half-life: about 6-8 days via albumin binding
frequency: typically once-weekly SubQ injection in community use
pulsatility: raises the baseline that the body's own GH rhythm sits on top of
extra chemistry: a maleimide linker on a C-terminal lysine that grabs albumin Cys34
best mental model: a continuous GH "tide" instead of a single pulse

why this distinction is not pedantic

CJC-1295-DAC at the standard weekly research dose of about 1 to 2 mg and CJC-1295 no-DAC at the standard daily dose of about 100 to 200 mcg represent very different loads on the GH axis. A vendor mislabel that swaps the two would deliver either ten times the intended weekly burden, or essentially no effect (Teichman et al. 2006; Sigalos and Pastuszak 2018).

For the rest of this course, every dose, half-life, or pulsatility claim explicitly names the variant. If a sentence does not say "no-DAC" or "DAC," assume it refers to both.

key terms

definitions for the technical words that show up across this course. tap to expand.

CJC-1295 peptide family

An umbrella name for two related synthetic peptides built on the GHRH(1-29) backbone with four shared substitutions (D-Ala2, Gln8, Ala15, Leu27). CJC-1295-DAC adds a maleimidopropionic-acid linker to a C-terminal lysine that binds plasma albumin in vivo; CJC-1295 no-DAC does not. The name alone does not specify the variant.

no-DAC variant drug form

Modified GRF(1-29), also called tetrasubstituted GRF(1-29). The CJC-1295 backbone without the DAC linker. Half-life is about 30 minutes in plasma. Community research dosing is roughly 100 to 200 mcg subcutaneously, one to three times daily. Functionally a stabilized sermorelin (Jetté et al. 2005).

DAC variant drug form

CJC-1295 with the Drug Affinity Complex linker: a maleimidopropionic-acid group on a C-terminal lysine that reacts with the free thiol of albumin Cys34 in vivo. The resulting albumin conjugate has an apparent half-life of about 6 to 8 days. Community research dosing is roughly 1 to 2 mg subcutaneously, once weekly (Teichman et al. 2006).

modified GRF(1-29) synonym

A commonly used name for CJC-1295 no-DAC. Sometimes written "mod GRF 1-29" or "tetrasubstituted GRF(1-29)." If you see modified GRF(1-29) in a forum or vendor listing, you should mentally translate it to CJC-1295 no-DAC. It is not the DAC variant.

GHRH hormone

Growth hormone-releasing hormone. A 44-residue hypothalamic peptide released into the pituitary portal circulation that asks somatotrope cells in the anterior pituitary to release a pulse of GH. Sometimes called GRF (growth-releasing factor) in older literature. CJC-1295 is a stabilized analog of its first 29 residues.

GHRHR receptor

The GHRH receptor. A class B G-protein-coupled receptor cloned in 1992 from rat pituitary by Kelly Mayo, expressed almost exclusively on pituitary somatotropes. Both CJC-1295 variants act here. Activation drives Gas, adenylyl cyclase, cAMP, PKA, CREB, and ultimately GH gene transcription and granule exocytosis (Mayo 1992).

GH hormone

Growth hormone, also called somatotropin. A 191-amino-acid protein hormone made and stored in pituitary somatotropes and released into the blood in pulses. GH acts on liver, muscle, adipose, and bone. Most of its long-range anabolic effects are mediated by IGF-1 downstream.

IGF-1 hormone

Insulin-like growth factor 1. A protein made mostly by the liver in response to GH, carried in blood by binding proteins including IGFBP-3 and the acid-labile subunit. IGF-1 mediates most growth-promoting and anabolic effects classically attributed to GH and is the standard exposure biomarker for chronic GH-axis interventions like CJC-1295.

albumin Cys34 target site

The single free thiol on serum albumin, located on cysteine 34 in domain I. This residue is the chemical anchor point for the CJC-1295-DAC maleimide linker. Albumin's normal half-life is about 19 days, sustained by FcRn-mediated cellular recycling, and the DAC conjugate borrows most of that kinetic envelope (Hoogenboezem and Duvall 2018).

half-life borrowing pk concept

The generalizable medicinal-chemistry trick at the heart of CJC-1295-DAC: attach a small bioactive peptide to a long-lived carrier protein and let the carrier dominate clearance. A free peptide below the renal-filtration cutoff clears in minutes; the same peptide tethered to albumin persists for days. Sermorelin, the no-DAC variant, and tesamorelin do not use this trick.

pulsatility physiology

The pattern of GH release as discrete bursts rather than a steady stream. In healthy adults GH pulses occur six to twelve times a day, with the largest one during slow-wave sleep. The no-DAC variant produces short pulses similar to native GHRH. The DAC variant raises the baseline on top of which the body's own pulsatility continues, per Ionescu and Frohman 2006.

tachyphylaxis pharmacology

A reduction in response after repeated or continuous agonist exposure, mediated by receptor desensitization, internalization, and beta-arrestin recruitment. GHRHR is a class B GPCR and follows this pattern. The concern is largest for CJC-1295-DAC, where the receptor sits occupied for days; community cycling protocols (8-12 weeks on, then off) are partly justified by this risk.

the dac linker, briefly

a quick walkthrough of how a single chemical handle on the c-terminus turns a 30-minute peptide into a 6-to-8-day one. unit 3 dissects the chemistry; this section is just the headline.

the chemical trick in one paragraph

The DAC linker is a small chemical handle called a maleimide, attached to the peptide through a short spacer. Maleimides are very selective for free thiol groups at body pH. Plasma albumin happens to have exactly one accessible free thiol, on cysteine 34, sitting on the outside of the protein.

After a subcutaneous CJC-1295-DAC injection, the peptide diffuses into the blood, finds albumin within hours, and forms a covalent bond there (Léger et al. 2004; Jetté et al. 2005). The peptide is now permanently riding on albumin until the whole complex is cleared.

1

free peptide

CJC-1295-DAC enters plasma carrying a reactive maleimide group on a C-terminal lysine.

2

albumin docks

The maleimide reacts with the single free thiol on albumin Cys34 and forms a covalent thioether bond.

3

long-circulating conjugate

The roughly 3.6 kDa peptide now rides a roughly 70 kDa carrier with a 19-day natural half-life.

why this matters for the rest of the course

Once the peptide is glued to albumin, it inherits most of albumin's pharmacokinetic envelope, including FcRn-mediated recycling through endothelial cells. The 3.6 kilodalton peptide alone would be filtered by the kidneys in minutes. As part of a roughly 70 kilodalton albumin complex, it persists for days (Hoogenboezem and Duvall 2018).

Unit 3 walks the maleimide mechanism step by step at the atomic level and explains why Léger et al. 2004 first validated this strategy with a GLP-1 conjugate before ConjuChem applied it to a GHRH analog. For now, the headline is enough: the DAC linker is the one chemical handle that turns CJC-1295 from a daily peptide into a weekly one.

interactive: variant toggle

switch between no-DAC and CJC-1295-DAC to compare half-life, dosing frequency, pulsatility, mass, and primary use case side by side.

no-DAC vs DAC variant toggle

tap to switch between the no-DAC and DAC variants and see how dose, half-life, and GH pulse shape change

the conjuchem development story

where cjc-1295 came from, why the dac platform was novel, and how a promising albumin-tethered ghrh analog ended up halted at phase ii.

conjuchem and the dac platform (~2004-2008)

CJC-1295 was developed by ConjuChem Biotechnologies, a Montreal company, in the early 2000s. Its proprietary Drug Affinity Complex platform was designed to solve a generic problem in peptide drug development: small peptides clear from blood in minutes, which forces continuous infusion or constant injections. ConjuChem first validated DAC chemistry with a GLP-1 analog called CJC-1131, then applied the same maleimide-Cys34 strategy to GHRH(1-29) to create CJC-1295-DAC (Léger et al. 2004; Jetté et al. 2005).

the long-acting ghrh hypothesis

The central pharmacologic hypothesis was that a long-acting GHRH analog could deliver sustained GH-axis stimulation without the side effects of recombinant GH. Sermorelin and native GHRH(1-29) had 3 to 10 minute half-lives, which made any sustained-elevation use case impractical. CJC-1295-DAC was meant to prove that an albumin-tethered GHRH peptide could keep IGF-1 elevated for a week per dose (Teichman et al. 2006).

teichman 2006: the one anchor trial

The pivotal evidence is a single Phase I single-ascending-dose study in healthy adults, published by Teichman and colleagues in 2006. A single subcutaneous CJC-1295-DAC dose produced 2- to 10-fold elevations in mean GH and 1.5- to 3-fold elevations in IGF-1 lasting 6 to 11 days. This is still the strongest direct CJC-1295 human dataset.

the phase ii halt

ConjuChem ran a Phase II trial in HIV-associated lipodystrophy (NCT00267527) enrolling 192 participants on weekly CJC-1295-DAC dose escalation. The study was halted in July 2006 after a cardiovascular death at an Argentina site. The on-site physician attributed the death to pre-existing coronary disease rather than the study drug, but ConjuChem discontinued development and no CJC-1295 trial has been registered since (NCT00267527; AIDSmap 2006).

why community stacks pick cjc-1295

cjc-1295 dominates community gh-axis stacks despite a thin trial record. understanding why is the regulatory and popularity hook for this course.

the practical pull

Among GHRH analogs reaching the gray-market peptide research-chemical economy, CJC-1295-DAC stands out for two practical reasons. Weekly dosing is more convenient than daily sermorelin or daily no-DAC injections. The Phase I data document real, measurable IGF-1 elevation for over a week per dose, which translates into a strong perceived effect (Teichman et al. 2006).

once-weekly DAC convenience

CJC-1295-DAC's roughly 6 to 8 day half-life means one injection per week instead of one to three injections per day. That single fact carries a lot of the pull for community users compared with sermorelin or the no-DAC variant.

measurable IGF-1 elevation

A single CJC-1295-DAC dose holds IGF-1 elevated for 9 to 11 days, per Teichman 2006. That is a real biomarker effect users can feel and (if they choose) measure, which anchors the molecule's reputation more solidly than purely anecdotal peptides.

the CJC + IPA stack story

The dominant community combination pairs CJC-1295 with ipamorelin, a selective ghrelin-receptor agonist. The synergy story rests on real human data showing GHRH plus GHRP combinations release more GH than either alone (Bowers et al. 1990; Raun et al. 1998).

FDA 503A Category 2 and WADA banned

CJC-1295 was placed in FDA 503A Category 2 in September 2023, flagging significant safety concerns; the 2024 removal was procedural, not safety-cleared (fda_503a_bulks). WADA names CJC-1295 explicitly under S2.2, prohibited in- and out-of-competition for all sports (WADA 2026).

WADA 2026 Prohibited List -- Section S2.2

"Growth hormone (GH), its fragments and releasing factors ... including CJC-1295 ... are prohibited at all times, in- and out-of-competition."
CJC-1295 is named explicitly on the WADA 2026 Prohibited List under section S2.2 (GH releasing factors). Any athlete subject to USADA, NCAA, or military testing inherits this prohibition (WADA 2026).

honest evidence ceiling

what is solid for cjc-1295, what is class-level extrapolation, what is community-level, and what has simply never been studied in adequately powered trials.

solid

phase i PK/PD of CJC-1295-DAC

A single Phase I trial directly characterizes the DAC variant in humans.

a single SubQ CJC-1295-DAC dose raised GH 2- to 10-fold and IGF-1 1.5- to 3-fold in healthy adults (Teichman et al. 2006).
IGF-1 elevation persisted 9-11 days per dose, consistent with the ~6-8 day half-life.
pulsatility was largely preserved under continuous GHRHR stimulation across multiple doses (Ionescu and Frohman 2006).

moderate

GHRH-analog class evidence via tesamorelin

The mechanism family CJC-1295 belongs to has at least one fully developed clinical proof-of-concept.

tesamorelin, a different GHRH analog, completed Phase III in HIV-associated lipodystrophy and reduced visceral fat by roughly 15% at 26 weeks (Falutz et al. 2007).
this validates the GHRH-analog drug class but does not validate CJC-1295 specifically.
once-daily CJC-1295 normalized growth in the GHRH-knockout mouse, supporting the receptor-level mechanism (Alba et al. 2006).

weak

community body-composition and recovery claims

Biologically plausible but extrapolated from sermorelin, rhGH, and tesamorelin literature, plus anecdote.

community CJC + IPA stack reports of lean-mass gain, fat reduction, and sleep depth rest on extrapolation, not direct CJC-1295 RCTs.
GH secretagogue use raised IGF-1 in hypogonadal men (Sigalos et al. 2017) but did not measure body composition with controls.
the broader healthy-elderly rhGH literature shows small body-composition shifts plus dose-limiting adverse events (Sigalos and Pastuszak 2018).

missing

modern controlled human RCTs of CJC-1295

As of 2026, none of the following exist at scale.

no completed Phase III trial; ConjuChem Phase II in HIV-lipodystrophy was halted in 2006 before pivotal readout (NCT00267527; AIDSmap 2006).
no head-to-head trial of CJC-1295 no-DAC vs DAC, or of either variant vs sermorelin or tesamorelin.
no controlled long-term safety dataset beyond the Phase II window.
no controlled trial of the CJC + IPA community stack or of CJC-1295 in adult GHD.

The most common mistake when reading about CJC-1295 online is treating tesamorelin trial results, rhGH studies, or sermorelin data as if they were CJC-1295 data. The Phase I PK/PD work is real for CJC-1295-DAC specifically. Almost every other claim rests on class-level extrapolation, on the halted Phase II program, or on community use. This course separates the four tiers carefully throughout, and the safety unit returns explicitly to the vendor-mislabeling risk that comes from collapsing the no-DAC and DAC variants into one name.

what you will learn

where this course goes from here.

The next nine units take this unit's overview and go much deeper. The chemistry unit dissects the modified GRF(1-29) backbone and the Lys30 maleimide linker. The DAC mechanism unit walks through the maleimide-Cys34 chemistry step by step.

The clinical evidence unit is the marquee unit and spends its whole runtime on the Teichman 2006 Phase I trial and the ConjuChem Phase II halt.

02

chemistry and structure

the modified GRF(1-29) backbone, the four substitutions (D-Ala2, Gln8, Ala15, Leu27), and the Lys30 maleimidopropionic linker that defines the DAC variant.
03

the DAC mechanism

deep dive on maleimide-cysteine chemistry, albumin Cys34 covalent binding, and how a roughly 3.6 kDa peptide inherits albumin's ~19-day half-life via FcRn recycling.
04

pulsatility vs sustained GH

why native GH is pulsatile, how the no-DAC variant amplifies natural pulses, how the DAC variant raises baseline GH continuously, and the tachyphylaxis question on chronic DAC dosing.
05

clinical evidence

the marquee evidence unit. Teichman 2006 Phase I PK/PD, Ionescu and Frohman 2006 pulsatility data, Alba 2006 GHRH-knockout-mouse rescue, and the ConjuChem Phase II HIV-lipodystrophy halt in detail.
06

stack strategy

Bowers 1990 GHRH plus GHRP synergy, the CJC plus ipamorelin community stack rationale, no-DAC vs DAC dose framing, and why CJC-1295 dominates community GH-axis stacks vs sermorelin.
07

CJC-1295 vs other GH-axis analogs

CJC-1295 (no-DAC and DAC) compared to sermorelin, tesamorelin (FDA-approved for HIV-lipodystrophy), ipamorelin, MK-677, and rhGH across mechanism, half-life, approval status, and evidence.
08

safety and product quality

tachyphylaxis on chronic DAC use, IGF-1 elevation and the acromegaly-shape risk, glucose handling, and the CJC-1295-unique no-DAC vs DAC vendor-mislabeling problem.
09

administration and regulatory status

subcutaneous dosing (once-weekly DAC vs 1-3x daily no-DAC), BAC water reconstitution, the FDA 503A Category 2 listing, and the WADA S2.2 prohibition.
10

final exam and certification

comprehensive exam covering all nine prior units. pass and earn a CJC-1295 Specialist certificate.

By the end you should be able to read a paper, a Reddit post, or a vendor page about CJC-1295 and immediately tell which claims have direct trial evidence behind them, which are extrapolated from tesamorelin or rhGH, and which are pure marketing. You should also never confuse the no-DAC and DAC variants again.

30

amino acid residues in the backbone

10

units including final exam

~3 hours

estimated to complete the course

certificate

awarded on passing the final exam

Knowledge Check

confirm the no-DAC vs DAC distinction, the DAC linker headline, the ConjuChem trial record, and the evidence-ceiling tiers before moving deeper.

Practice

reinforce the distinctions that matter most for the rest of the course.

what is cjc-1295?