CJC-1295 With DAC vs No DAC: Why Identity Matters

The trade name “CJC-1295” is not enough to know which molecule is in hand. The principal human literature and FDA’s compounding review include forms with a drug-affinity complex and forms described as lacking that complex. Collapsing them turns a long-acting trial into a product card that is not that material.^1,6,5

The cluster map is in CJC-1295 + Ipamorelin: component evidence vs blend evidence. This page stays with the identity of the CJC component.

What DAC means

DAC is not a synonym for “better” or “approved.” It is a chemical modification with a pharmacological purpose: changing how long the analogue circulates. Teichman and colleagues described CJC-1295 as a long-acting analogue of growth hormone-releasing hormone. That sentence belongs to the form designed for prolonged exposure, not to every label that says CJC-1295.¹

“No DAC” or “without DAC” names, in catalogs and reviews, an analogue that does not carry that complex. A 2026 review of unapproved GH-IGF-I-axis peptides explicitly distinguishes the DAC form from the non-DAC form and the gap between clinical research and self-administration. Distinguishing the two is not proof that they are equivalent.⁵

Albumin binding

Albumin is an abundant plasma protein. An analogue built to bind it does not circulate as the peptide fragment alone. The design changes residence time and, with it, the exposure curve. That is why the 2006 literature speaks of prolonged stimulation of GH and IGF-I: it was measuring a form built to last.¹

That binding is not inherited by the name. If the material does not carry the complex, it cannot be asserted to bind albumin in the same way. In the sources reviewed as of September 1, 2026, we did not identify a human trial that measured the same long-acting pharmacokinetics in a material declared to have no DAC.^1,5

When FDA evaluated related bulk substances, it did not treat “CJC-1295” as a single chemical entity. It reviewed free base, acetate, and several DAC forms separately. That administrative separation confirms that identity is not an interchangeable nickname.^6,7

Why exposure differs

Exposure, here, means how much analogue the body sees and for how long. Two materials can share a GRF fragment and still produce different curves if one is designed to bind albumin and the other is not. Copying the trial’s name does not copy the curve.

The human endpoints published in 2006 — GH, IGF-I, and pharmacokinetics — describe that long-acting exposure. Ionescu and Frohman, the same year, studied GH pulsatility under continuous stimulation by the long-acting analogue. Neither paper turns a “no DAC” lot into the studied object.^1,2

A GH or IGF-I increase is also not muscle gain, fat loss, recovery, anti-aging, sleep, or performance. It is an endocrine biomarker measured in healthy adults under a defined protocol. Form identity comes before any biomarker reading.^1,2

Long-acting human studies

Teichman and colleagues published two randomized, placebo-controlled, double-blind ascending-dose studies in 2006 in healthy adults aged 21 to 61 years. Endpoints were GH, IGF-I, and pharmacokinetics of the long-acting form. They observed sustained GH and IGF-I increases. That is pharmacology of a DAC form, not a body-composition trial and not a trial of the Ipamorelin blend.¹

Ionescu and Frohman showed that pulsatile GH secretion persisted during continuous stimulation by that analogue in healthy men. Sackmann-Sala and colleagues analyzed serum protein profiles in samples from an existing cohort; it is not an independent efficacy trial.^2,3

NCT00267527 is a Phase 2 registry record in patients with HIV and visceral obesity. The status is Terminated. The last update posted on the registry is 16 October 2006. No results are posted. The registry record alone does not establish why the study stopped.⁴

Short-duration tolerability in healthy adults is not the same as “proven safe.” FDA later identified safety uncertainties and limited clinical data, and identified serious adverse events including increased heart rate and systemic vasodilatory reaction. That is not summarized here as “CJC causes heart problems.”^1,6,9

The inventory of those papers is in CJC-1295 in humans. This page needs only one fact: those studies are not, by the name alone, studies of a no-DAC material.

FDA definitions

Those five entries are not chemically identical. Pharmacokinetic data should not be silently transferred among them. The advisory committee voted on the nominations; FDA had proposed against inclusion on the 503A list. An advisory vote is not a drug ban and is not an approval.^6,7,8

The official bulk-substance page describes the 503A list, the 2019 final rule, and the interim category policy. Being nominated, sitting in a category, or leaving a category because a nomination was withdrawn does not make CJC-1295 an approved drug.⁸

As of September 1, 2026, CJC-1295 appears on the withdrawn-nomination table of the compounding-risks page. That entry mentions immunogenicity, impurity characterization, increased heart rate, and systemic vasodilatory reaction, with limited human data. The scope is U.S. compounding, not a clinical card for a research vial.⁹

No-DAC naming

Catalogs and online copy use “CJC-1295 without DAC,” “CJC-1295 no DAC,” and nearby phrases. FDA documented identity and naming inconsistencies in the nominations. Those labels are not perfectly standardized synonyms.^6,5

A “no DAC” label is an identity claim, not a measurement. It does not, by itself, prove that the lot lacks the complex, that it matches a published sequence, or that it does or does not reproduce 2006 exposure. The lot certificate of analysis is the analytical document; this page does not replace it.

“No DAC” also cannot be read as if a parallel human clinical body already existed next to Teichman. In the sources reviewed as of September 1, 2026, we did not identify a published human program that equivalently characterized a no-DAC material with the same long-acting GH, IGF-I, and pharmacokinetic endpoints.^1,5

Mod GRF terminology

“Modified GRF(1-29)” and “Mod GRF 1-29” circulate as names for an analogue with substitutions relative to the native fragment. In commerce they are often tied to a CJC described as no DAC. That catalog association does not standardize the sequence or prove that two suppliers sell the same entity.^5,6

Peptra’s catalog uses “modified GRF(1-29) analog” for the CJC component it identifies as CJC-1295 (No DAC). That is the product-identity claim. This page does not invent a different DAC status, does not treat “Mod GRF” as an official FDA name, and does not claim chemical identity with the 2006 DAC material.

If a paper names CJC-1295 and describes long action or albumin binding, that paper’s object does not transfer to a material labeled Mod GRF with no DAC. The nomenclature explains fragment kinship; it does not equalize exposure.^1,5

Half-life cannot transfer

The half-life and pharmacokinetics published for the DAC form belong to that form. They cannot be copied onto a no-DAC material, or onto a commercial lot merely because the trade name says CJC-1295. The 2026 review stresses that gap between what was studied and what is self-administered.^1,5

DAC half-life also does not transfer to the blend. In the sources reviewed as of September 1, 2026, we did not identify a human trial that administered CJC-1295 and Ipamorelin together, and therefore there is no exact-pair exposure curve to inherit.¹

• Teichman 2006 pharmacology describes a long-acting DAC form.¹
• Ionescu 2006 pulsatility was measured under that long-acting analogue.²
• Sackmann-Sala 2009 used samples from an existing cohort, not a new no-DAC material.³
• NCT00267527 is Terminated, with no results posted, and does not fill in pharmacokinetics for a no-DAC lot.⁴

What Peptra identifies

Peptra’s current catalog identifies the vial’s CJC component as CJC-1295 (No DAC), a modified GRF(1-29) analog, 10 mg together with 10 mg of ipamorelin. The product name is “CJC-1295 / Ipamorelin.” That is a product-identity claim, not a confirmation that the lot matches the DAC material used in the 2006 trials.

This page does not invent a DAC status beyond what the catalog claims. It does not assert that the vial is the form Teichman studied, that it reproduces that half-life, or that ipamorelin in the same vial creates pair evidence. The blend question is in whether combination evidence exists.

A certificate of analysis can report identity and purity of the released material. It does not prove that DAC pharmacokinetics apply, does not prove synergy, and does not authorize a human use. Anyone comparing a 2006 paper with this vial has to compare the form, not only the trade name.

If the question is what was measured in people with the long-acting form, continue to CJC-1295 in humans. The cluster index remains the CJC-1295 + Ipamorelin hub.