Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of CJC-1295 (no DAC) and IGF-1 LR3 — mechanism, dosing, side effects, legal status, and pricing.
CJC-1295 without Drug Affinity Complex (no DAC), also known as Modified GRF(1-29), is a synthetic analog of the first 29 amino acids of growth hormone-releasing hormone (GHRH). Four amino acid substitutions at positions 2, 8, 15, and 27 confer resistance to DPP-IV enzymatic degradation while maintaining GHRH-receptor binding activity. Unlike the DAC-conjugated variant (half-life 6–8 days via albumin binding), the no-DAC form has a short half-life of approximately 30 minutes, producing brief, pulsatile bursts of GH secretion. Not FDA-approved in any form.
IGF-1 LR3 is an 83-amino-acid modified IGF-1 analog with a 13-residue N-terminal extension (MFPAMPLSSLFVN) and an Arg-3 substitution. These modifications reduce binding to IGF binding proteins (IGFBPs), extending effective half-life and increasing tissue bioavailability relative to native IGF-1. It is a research/cell-culture reagent and is NOT FDA-approved for any human use. Do not confuse with mecasermin (Increlex), which is recombinant human IGF-1 and IS FDA-approved for severe primary IGF-1 deficiency.
CJC-1295 (no DAC)
IGF-1 LR3
Category
Legal Status
Mechanism
Dose Range
Route
Frequency
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
CJC-1295 (no DAC)
IGF-1 LR3
COA corpus from Disclosed Labs — independently tested batches only.
CJC-1295 (no DAC)
2
COAs
99.4%
Avg purity
2
Labs
IGF-1 LR3
42
COAs
98.7%
Avg purity
9
Labs
The parent molecule CJC-1295 (DAC form) was identified by Jetté et al. (Endocrinology, 2005; PMID 15817669) at ConjuChem as a tetrasubstituted GHRH(1-29) bioconjugate that covalently binds Cys34 of serum albumin via a maleimidopropionyl-lysine linker, extending half-life to roughly 5.8–8.1 days. In healthy adults, Teichman et al. (JCEM, 2006; PMID 16352683) showed single SubQ doses of the DAC form produced 2- to 10-fold GH elevations for ≥6 days and 1.5- to 3-fold IGF-1 elevations for 9–11 days, and Ionescu & Frohman (JCEM, 2006; PMID 17018654) demonstrated that pulsatile GH secretion was preserved (7.5-fold increase in trough GH, IGF-1 up 45%). ConjuChem halted Phase 2 lipodystrophy development around 2006–2007 after a participant death in an HIV-visceral-adiposity trial (deemed by the trial physician most likely due to pre-existing coronary artery disease rather than CJC-1295, but the program was not resumed; aidsmap news, July 2006). The no-DAC form described here ('Modified GRF 1-29') shares the same position-2/8/15/27 substitutions (which confer DPP-IV resistance; see Soule et al., JCEM 1994, PMID 7962295 for the foundational D-Ala2 half-life work) but omits the albumin-linker lysine, giving a short (~30 min) half-life similar to sermorelin. No form of CJC-1295 is FDA-approved for any indication. Grey-market compounding practice pairs the no-DAC form with ipamorelin; this combination is not clinically validated for anti-aging, body composition, or performance use, and peer-reviewed human trials of the no-DAC variant specifically are lacking — the 100–300 mcg dosing range reflects community practice, not clinical evidence.
Key references
CJC-1295 (no DAC) and IGF-1 LR3 are both in the Performance category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Dosing Notes
Half-life
Side Effects
Contraindications
Lab Testing
Francis et al. (J Mol Endocrinol 1992; PMID 1378742) characterized LR3-IGF-1 as a fusion analog whose enhanced biological potency derives from reduced IGFBP binding; in IGFBP-free cell systems LR3 was actually LESS potent than native IGF-1, underscoring that the 'potency' is really reduced sequestration rather than intrinsically stronger receptor activation. Tomas (Growth Horm IGF Res 2001; PMID 11472075) infused LR(3)IGF-I into food-restricted rats and found it preserved body weight and nitrogen retention but did NOT conserve skeletal muscle protein — which contradicts the common 'potent muscle builder' framing from preclinical literature alone. There are no controlled human trials supporting bodybuilding use. Epidemiologic and mechanistic work reviewed by Grimberg (Cancer Biol Ther 2003; PMID 14688466) links elevated IGF-1 axis activity to breast, prostate, and colorectal cancer risk, so chronic systemic LR3 exposure carries a concrete — not merely theoretical — tumorigenesis concern. IGF-1 and its analogs are banned at all times under the WADA Code.
Key references
Disclosed Labs