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CJC-1295 No DAC vs CJC-1295 DAC

The two forms share an identical GHRH(1-29) backbone with the same four amino acid substitutions. The Drug Affinity Complex (DAC) — a single maleimidopropionic acid linker that covalently binds serum albumin — is the only chemical difference. Every downstream pharmacologic property flows from that one addition. This page reads out those differences precisely.

Last reviewed 2026-07-12

  • Chemical difference

    CJC-1295 (No DAC)

    Modified GRF(1-29): D-Ala², Gln⁸, Ala¹⁵, Leu²⁷. No C-terminal linker.

    CJC-1295 DAC

    Same Modified GRF(1-29) backbone + a maleimidopropionic acid (MPA) linker at the C-terminus that covalently binds serum albumin's cysteine-34 residue.

    1 citation in this row

  • Plasma half-life

    CJC-1295 (No DAC)

    ~30 minutes

    CJC-1295 DAC

    ~5.8 to 8.1 days (Teichman JCEM 2006) — a >300-fold extension attributable to albumin conjugation

    1 citation in this row

  • Pharmacologic signal shape

    CJC-1295 (No DAC)

    Physiologic pulse: circulating drug concentration falls fast enough between doses for the pituitary to reset. GH pulse pattern resembles the endogenous rhythm.

    CJC-1295 DAC

    Sustained plateau: circulating drug concentration remains elevated across the dosing interval. Somatotroph-intrinsic pulses of GH still occur (Ionescu 2006), but they ride on top of a raised baseline.

    1 citation in this row

  • Dosing frequency

    CJC-1295 (No DAC)

    Once daily to 3× daily in research contexts, aligning with the natural nocturnal GH pulse.

    CJC-1295 DAC

    Once weekly, or every other week at higher doses. Daily dosing accumulates supraphysiologically within a week.

    1 citation in this row

  • IGF-1 elevation profile

    CJC-1295 (No DAC)

    IGF-1 elevations track the GH pulses — transient and modest. Chronic IGF-1 accumulation is less pronounced than with sustained-exposure forms.

    CJC-1295 DAC

    IGF-1 stays elevated across the ~1-week dosing interval. Sustained elevation is the mechanistic driver of the DAC form's characteristic side effects.

    1 citation in this row

  • Tolerability profile

    CJC-1295 (No DAC)

    Injection-site reactions, mild flushing, modest water retention with sustained daily use.

    CJC-1295 DAC

    More pronounced water retention, joint pain, and paresthesia (carpal-tunnel-like symptoms) attributable to sustained IGF-1 exposure across the dosing interval.

    1 citation in this row

  • Human evidence base

    CJC-1295 (No DAC)

    Limited modern controlled human data. Alba 2006 in GHRH-knockout mice supports receptor-level mechanism. The 'famous' CJC-1295 human papers (Teichman, Ionescu 2006) are not about this form.

    CJC-1295 DAC

    This is where Teichman JCEM 2006 and Ionescu JCEM 2006 belong. Dose-ranging phase-1 data in healthy adults; the pulsatile-under-continuous-stimulation finding; the ~8-day half-life figure that general sources attribute to 'CJC-1295' broadly.

    3 citations in this row

  • Commercial history

    CJC-1295 (No DAC)

    Intermediate in ConjuChem's development program, not the target product. Never advanced under this identity.

    CJC-1295 DAC

    The intended commercial product. Taken through phase-1 by ConjuChem; phase-2 was planned but not substantially advanced. ConjuChem went into bankruptcy protection in 2011 and no subsequent sponsor has picked up development.

The most useful way to think about the two forms of CJC-1295 is not as 'short-acting' and 'long-acting' versions of the same drug, but as two different drugs that happen to share a peptide backbone. One MPA linker changes what the receptor is signalling. The dosing frequency, the IGF-1 profile, the tolerability trade-offs, and even the commercial trajectory all trace back to that single chemistry difference. Neither compound is a substitute for a clinical decision informed by an individual's medical history.

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