CJC-1295 Without DAC + Ipamorelin | Buy Research-Grade Combination Peptide in Europe | ≥99% Purity

CJC-1295 Without DAC (Modified GRF 1-29) + Ipamorelin is a synergistic dual-peptide combination of a GHRH analogue and a selective GH secretagogue, available to buy in Europe for laboratory research into growth hormone pulse physiology, GHRH/GHRP synergy mechanisms, somatotroph biology, GH axis pharmacology, and the comparative study of pulsatile versus tonic GH secretion patterns.

Laboratories and research institutions across the EU can order verified, research-grade CJC-1295 Without DAC + Ipamorelin with fast international dispatch to Europe, full batch documentation, and ≥99% purity confirmed by HPLC and Mass Spectrometry on both peptide components.

✅ ≥99% Purity — HPLC & Mass Spectrometry Verified (Both Components)

✅ Batch-Specific Certificate of Analysis (CoA)

✅ Sterile Lyophilised Powder | GMP Manufactured

✅ Fast Dispatch to EU & Europe | Tracked Shipping

What is CJC-1295 Without DAC + Ipamorelin?

CJC-1295 Without DAC + Ipamorelin is a research combination pairing two mechanistically complementary GH axis peptides — a GHRH receptor agonist and a GHS-R1a agonist — that act through distinct and synergistic pituitary pathways to produce amplified, physiologically patterned pulsatile GH release exceeding that achievable through either peptide alone.

CJC-1295 Without DAC (also designated Modified GRF 1-29, or Mod-GRF 1-29) is a tetrasubstituted analogue of the natural GHRH(1-29)NH₂ sequence — incorporating four amino acid substitutions (Ala², Ala⁸, Gln¹⁵, Ala²⁷; with the His at position 1 substituted and D-Ala at position 2) designed to confer metabolic stability against dipeptidyl peptidase IV (DPP-IV) cleavage and endopeptidase degradation without the albumin-binding Drug Affinity Complex (DAC) modification present in CJC-1295 With DAC. The result is a short-acting GHRH receptor (GHRH-R) agonist with a plasma half-life of approximately 30 minutes — substantially longer than native GHRH(1-29) (half-life <5 minutes) but retaining the pulsatile, physiologically transient pharmacokinetic profile absent from the long-acting DAC variant. CJC-1295 Without DAC signals through GHRH-R/Gs/adenylyl cyclase/cAMP, driving cAMP-dependent PKA activation in somatotrophs and increasing intracellular calcium to stimulate GH gene transcription and secretory granule release.

Ipamorelin is a synthetic pentapeptide GH secretagogue (Aib-His-D-2-Nal-D-Phe-Lys-NH₂) and selective GHS-R1a (ghrelin receptor) agonist, distinguished within the GHRP class by its exceptional selectivity for GH release with minimal co-stimulation of cortisol, prolactin, or ACTH. Ipamorelin acts through GHS-R1a/Gq/phospholipase C/IP₃/calcium signalling in pituitary somatotrophs — a pathway mechanistically distinct from and complementary to the GHRH-R/cAMP pathway engaged by CJC-1295 Without DAC. The Aib³ substitution (α-aminoisobutyric acid) that distinguishes Ipamorelin from other GHRPs is the primary structural determinant of its selectivity — reducing interactions with hypothalamic CRH neurons that drive cortisol co-stimulation in less selective GHRPs such as GHRP-2 and Hexarelin.

When co-administered, CJC-1295 Without DAC and Ipamorelin engage complementary and convergent signalling pathways in pituitary somatotrophs — cAMP/PKA from GHRH-R activation and IP₃/calcium from GHS-R1a activation — producing synergistic intracellular signal amplification that drives GH release substantially exceeding the additive sum of either peptide individually. This mechanistic synergy, first characterised in foundational studies of GHRH and GHRP co-administration, provides the physiological and pharmacological rationale for the combination as a research tool for studying maximal physiological GH pulse generation and GH axis pharmacology.

What Does CJC-1295 Without DAC + Ipamorelin Do in Research?

In laboratory settings, the CJC-1295 Without DAC + Ipamorelin combination is studied across GH axis pharmacology, pituitary biology, GHRH/GHRP synergy mechanisms, somatotroph signalling, and comparative secretagogue research. EU and European researchers working with this combination typically focus on:

GHRH/GHRP synergy mechanism research — The co-administration of GHRH-R and GHS-R1a agonists produces GH release that is superadditive — exceeding the sum of the individual peptide responses — through convergent activation of the cAMP/PKA (GHRH-R) and IP₃/calcium (GHS-R1a) signalling axes in somatotrophs. Studies use the CJC-1295 Without DAC + Ipamorelin combination to examine the mechanistic basis of GHRH/GHRP synergy — characterising cAMP/calcium signal integration, the role of GHS-R1a in amplifying GHRH-driven cAMP responses, and the pituitary intracellular signalling nodes at which the two pathways converge to produce amplified GH secretory responses.

Pulsatile GH secretion physiology research — Physiological GH secretion occurs in discrete high-amplitude pulses driven by hypothalamic GHRH/somatostatin alternation. CJC-1295 Without DAC’s short pharmacokinetic profile preserves the pulsatile GH release pattern — producing transient, high-amplitude GH peaks that recapitulate the physiological pulse morphology absent from long-acting GHRH analogues with DAC modification. Studies use the combination to model pharmacological pulsatile GH secretion, examining pulse amplitude, duration, and inter-pulse interval — providing a research tool for studying the consequences of pulsatile versus tonic GH release profiles on downstream IGF-1 production and GH target tissue responses.

Somatotroph cell biology and GH secretion mechanisms — Studies in isolated somatotroph preparations, pituitary cell lines, and primary pituitary cultures use the CJC-1295 Without DAC + Ipamorelin combination to examine the cellular mechanisms of GH secretory granule fusion, exocytosis regulation, and the intracellular signalling events linking GHRH-R and GHS-R1a co-activation to GH release — including cAMP/PKA-mediated granule priming and IP₃/calcium-driven secretory granule fusion.

GH axis pharmacology and secretagogue potency research — The combination is used as a reference dual-pathway GH axis stimulus in comparative secretagogue pharmacology studies — providing a reproducible, mechanistically defined maximal GH-releasing stimulus against which the efficacy of alternative secretagogue combinations, dosing strategies, and GH axis modulators can be benchmarked. Studies characterising the potency, selectivity, and pharmacodynamic profiles of novel GH secretagogues routinely use the GHRH analogue + GHS-R1a agonist combination format as the reference stimulus design.

GH selectivity and HPA axis co-stimulation research — Ipamorelin’s exceptional GH selectivity — minimal cortisol, prolactin, and ACTH co-stimulation compared to GHRP-2, GHRP-6, and Hexarelin — makes the CJC-1295 Without DAC + Ipamorelin combination the most GH-selective GHRH/GHRP research pairing. Studies examining the relationship between GHS-R1a engagement selectivity and HPA axis co-activation use Ipamorelin as the reference selective GHRP — characterising how the Aib³ selectivity-conferring substitution eliminates hypothalamic CRH co-stimulation without compromising somatotroph GHS-R1a engagement and GH release potency.

IGF-1 axis and downstream GH biology research — GH released by CJC-1295 Without DAC + Ipamorelin stimulation drives hepatic IGF-1 production — the primary mediator of GH’s anabolic, growth-promoting, and metabolic effects. Studies use the combination to examine GH pulse amplitude-dependent IGF-1 production, IGF-1R signalling dynamics, and the downstream consequences of pharmacologically amplified GH pulsatility on target tissue responses — providing a research tool for studying the GH/IGF-1 axis without the confounding cortisol co-secretion that would accompany use of less selective GHRPs.

Comparative GHRH analogue pharmacology — With DAC versus Without DAC — Studies systematically comparing CJC-1295 Without DAC and CJC-1295 With DAC characterise the consequences of pharmacokinetic profile on GH secretion pattern — the transient pulsatile GH release produced by Mod-GRF 1-29 versus the sustained tonic GH elevation produced by the long-acting DAC variant. These comparative studies examine GH pulse physiology, somatotroph desensitisation, IGF-1 production kinetics, and the biological consequences of pulsatile versus continuous GH receptor stimulation in GH target tissues.

Somatostatin interaction and GH pulse gating research — Hypothalamic somatostatin tonically suppresses GH release and gates the timing of GH pulses through SSTR2/SSTR5 receptor signalling in somatotrophs. GHS-R1a agonism by Ipamorelin partially overcomes somatostatin suppression — a property characterised across the GHRP class. Studies use the CJC-1295 Without DAC + Ipamorelin combination to examine the interaction between GHS-R1a activation, somatostatin pathway suppression, and GHRH-R co-stimulation in determining GH pulse amplitude and somatostatin-override capacity.

GH deficiency and somatotroph reserve assessment research — Pharmacological stimulation of GH release by GHRH + GHRP combination is a well-characterised approach for assessing somatotroph GH secretory reserve — distinguishing hypothalamic GH deficiency (GHRH/GHRP responsive) from pituitary GH deficiency (GHRH/GHRP unresponsive). Studies use the CJC-1295 Without DAC + Ipamorelin combination to examine somatotroph reserve in pre-clinical models of GH axis pathology — providing mechanistic insight into the pituitary versus hypothalamic determinants of GH secretory capacity.

Ageing and age-associated GH decline research — GH pulse amplitude and frequency decline progressively with age — a phenomenon termed somatopause — associated with reduced GHRH drive and increased somatostatin tone. Studies use the CJC-1295 Without DAC + Ipamorelin combination in aged animal models to examine residual somatotroph GH secretory capacity, the reversibility of age-associated GH decline through pharmacological stimulation, and the downstream consequences of GH pulse restoration on IGF-1 levels and GH-dependent tissue biology.

Receptor desensitisation and resensitisation kinetics — Repeated or continuous GHRH-R and GHS-R1a stimulation produces receptor desensitisation and attenuated GH responses through distinct receptor-level mechanisms. Studies use the combination to characterise the kinetics of dual-receptor desensitisation — examining GHRH-R versus GHS-R1a desensitisation time courses, the differential contributions of each receptor to the declining GH response with repeated stimulation, and the recovery kinetics of somatotroph responsiveness following stimulation washout.

Body composition and metabolic research — GH released by CJC-1295 Without DAC + Ipamorelin stimulation drives lipolysis in adipocytes, protein synthesis in muscle, and gluconeogenesis in the liver — the primary metabolic consequences of GH pulse elevation. Studies in pre-clinical metabolic research models use the combination to examine the body composition and metabolic consequences of pharmacologically amplified GH pulsatility — characterising GH-dependent lipolysis, lean mass accretion, and insulin sensitivity changes in response to secretagogue-driven GH axis stimulation.

All research applications are for in vitro and pre-clinical use only.

What Do Studies Say About CJC-1295 Without DAC + Ipamorelin?

The CJC-1295 Without DAC + Ipamorelin combination draws on two well-developed independent research literatures — the GHRH analogue pharmacology literature characterising Mod-GRF 1-29 and related GHRH peptides, and the GHRP/GHS-R1a literature characterising Ipamorelin’s selectivity and GH-releasing biology — alongside a body of combinatorial GHRH/GHRP research establishing the mechanistic basis of secretagogue synergy.

GHRH/GHRP synergy characterisation: Foundational studies by Bowers, Thorner, and colleagues established that GHRH and synthetic GHRPs act through complementary pituitary signalling pathways — cAMP and calcium respectively — to produce synergistic GH release substantially exceeding that of either stimulus alone. These synergy studies established the mechanistic principle underpinning the GHRH analogue + GHS-R1a agonist combination format — demonstrating that dual-pathway somatotroph co-stimulation is not merely additive but produces signal amplification through convergent intracellular mechanisms. The CJC-1295 Without DAC + Ipamorelin combination applies this established synergy principle using half-life-optimised analogues of both component peptide classes.

CJC-1295 Without DAC (Mod-GRF 1-29) pharmacological characterisation: Studies characterising the tetrasubstituted Mod-GRF 1-29 sequence established that the four amino acid substitutions produce a DPP-IV-resistant, endopeptidase-stable GHRH analogue with approximately 30-minute plasma half-life — substantially extended versus native GHRH(1-29) without the albumin-binding continuous release profile of the DAC variant. These pharmacokinetic characterisation studies established Mod-GRF 1-29 as the short-acting GHRH analogue of choice for research applications requiring pulsatile GH release patterns, and documented its full GHRH-R agonism and cAMP-driven somatotroph activation equivalent to native GHRH.

Ipamorelin selectivity characterisation: Landmark studies by Raun, Sehested Hansen, and colleagues at Novo Nordisk characterised Ipamorelin as the first GHRP with a selectivity profile resembling GH-releasing hormone — producing robust GH release with essentially no elevation of cortisol, ACTH, or prolactin at doses producing maximal GH responses. These selectivity studies documented that the Aib³ substitution is the critical structural determinant of Ipamorelin’s selectivity, eliminating hypothalamic CRH co-stimulation while preserving full somatotroph GHS-R1a engagement — establishing Ipamorelin as the reference selective GHRP against which the HPA axis co-stimulation profiles of other GHRPs are benchmarked.

Pulsatile versus tonic GH release biology: Studies comparing the downstream biological consequences of pulsatile GH release (produced by short-acting GHRH analogues and GHRPs) versus tonic GH elevation (produced by long-acting GHRH-DAC variants or continuous GH infusion) established that pulsatile GH patterns are more potent drivers of hepatic IGF-1 production and anabolic GH signalling than equivalent total GH doses delivered continuously — providing the physiological rationale for preserving pulsatile GH release characteristics in GH secretagogue research designs.

GH axis stimulation in pre-clinical ageing models: Studies examining GHRH analogue + GHRP combinations in aged rodent models documented restoration of GH pulse amplitude and IGF-1 levels toward younger values — with findings establishing that somatotroph GH secretory capacity is largely preserved in aged animals despite reduced hypothalamic GHRH drive, and that pharmacological dual-pathway somatotroph stimulation can overcome age-associated GH decline. These ageing studies provided mechanistic context for interpreting somatopause biology and the somatotroph reserve concept.

Comparative GHRP co-stimulation studies: Studies systematically comparing GH secretagogue selectivity profiles — Ipamorelin, GHRP-6, GHRP-2, and Hexarelin — in combination with GHRH analogues documented that GH synergy with GHRH is maintained across the GHRP selectivity spectrum, while cortisol co-stimulation varies dramatically by GHRP identity. These comparative combination studies established that Ipamorelin provides the GH synergy of the GHRH/GHRP combination format without the confounding HPA axis co-activation that complicates interpretation of studies using less selective GHRPs.

CJC-1295 Without DAC + Ipamorelin vs Related GH Axis Research Combinations

Combination	GHRH Component	GHRP Component	GH Selectivity	Pulse Pattern	Key Research Distinction
CJC-1295 w/o DAC + Ipamorelin	Mod-GRF 1-29 (t½ ~30 min)	Ipamorelin — GHS-R1a selective	Highest — minimal cortisol/prolactin	Pulsatile	Most selective GHRH/GHRP combination; reference for clean GH axis stimulation
CJC-1295 With DAC + Ipamorelin	CJC-1295 DAC (t½ ~8 days)	Ipamorelin — GHS-R1a selective	High	Sustained/tonic	Long-acting GHRH + selective GHRP; blunted pulsatility
CJC-1295 w/o DAC + GHRP-2	Mod-GRF 1-29 (t½ ~30 min)	GHRP-2 — high potency	Moderate — cortisol/prolactin elevation	Pulsatile	Higher GH potency; HPA axis co-activation — less clean profile
CJC-1295 w/o DAC + GHRP-6	Mod-GRF 1-29 (t½ ~30 min)	GHRP-6 — reference GHRP	Moderate — appetite, cortisol	Pulsatile	Reference GHRH/GHRP combination; appetite biology co-stimulation
CJC-1295 w/o DAC + Hexarelin	Mod-GRF 1-29 (t½ ~30 min)	Hexarelin — highest potency GHRP	Lower — strong HPA co-activation	Pulsatile	Highest GH potency combination; cardioprotection + GH axis
Native GHRH(1-29) + Ipamorelin	Native GHRH(1-29) (t½ <5 min)	Ipamorelin — selective	Highest	Very short pulse	Reference native ligand combination; rapid clearance limits utility
MK-677 (Ibutamoren)	None — oral GHS-R1a agonist	GHS-R1a non-peptide	Moderate	Tonic elevation	Oral administration research; sustained GH/IGF-1 elevation

Component Peptide Profiles

CJC-1295 Without DAC (Modified GRF 1-29)

Parameter	Detail
Sequence	Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-NH₂
Modifications	Ala², Ala⁸, Gln¹⁵, Ala²⁷ substitutions — DPP-IV resistance; no DAC modification
Receptor	GHRH-R (Growth Hormone-Releasing Hormone Receptor)
Signalling	Gs/adenylyl cyclase/cAMP/PKA
Half-life	~30 minutes (vs <5 min for native GHRH)
GH release pattern	Pulsatile — transient high-amplitude pulse
Cortisol/Prolactin	None

Ipamorelin

Parameter	Detail
Sequence	Aib-His-D-2-Nal-D-Phe-Lys-NH₂
Key Structural Feature	Aib³ (α-aminoisobutyric acid) — selectivity-conferring substitution
Receptor	GHS-R1a (Ghrelin Receptor)
Signalling	Gq/phospholipase C/IP₃/calcium
Half-life	~2 hours
GH release pattern	Pulsatile — GH selective
Cortisol/Prolactin	Minimal — most selective GHRP
GHRP Class Position	Most GH-selective member of the GHRP family

Buying CJC-1295 Without DAC + Ipamorelin in Europe — What’s Included

Every order dispatched to EU and European research institutions includes:

• Batch-Specific Certificate of Analysis (CoA) — both components
• HPLC Chromatogram — both components
• Mass Spectrometry Confirmation — both components
• Sterility and Endotoxin Testing Reports
• Reconstitution Protocol
• Technical Research Support

Frequently Asked Questions — CJC-1295 Without DAC + Ipamorelin EU

Can I Buy CJC-1295 Without DAC + Ipamorelin in the EU and Europe?

Yes. We supply both peptides as research-grade compounds with fast tracked dispatch to all EU member states and wider European destinations. All orders include full batch documentation for both components. Peptides are supplied strictly for laboratory research use only.

What is the Difference Between CJC-1295 Without DAC and CJC-1295 With DAC?

The critical difference is pharmacokinetic profile and the resulting GH secretion pattern. CJC-1295 Without DAC (Mod-GRF 1-29) lacks the Drug Affinity Complex albumin-binding modification, producing a short plasma half-life of approximately 30 minutes and a transient, pulsatile GH release pattern that recapitulates physiological GH pulse morphology. CJC-1295 With DAC incorporates a reactive NHS-ester maleimide group that binds covalently to circulating albumin — extending plasma half-life to approximately 6–8 days and producing sustained, tonic GH elevation. For research applications requiring physiological pulsatile GH release patterns, CJC-1295 Without DAC is the appropriate analogue; CJC-1295 With DAC is used when sustained GH axis elevation and elevated baseline IGF-1 are the research objective.

Why is Ipamorelin Considered the Most Selective GHRP?

Ipamorelin’s selectivity for GH release over cortisol, ACTH, and prolactin co-stimulation is conferred primarily by its Aib³ (α-aminoisobutyric acid) substitution — a non-natural alpha-methyl amino acid that constrains the peptide backbone conformation in a manner that optimises GHS-R1a engagement at somatotrophs while reducing interactions with GHS-R1a expressing hypothalamic CRH neurons responsible for ACTH/cortisol co-stimulation. Studies have documented that Ipamorelin produces cortisol and prolactin responses statistically indistinguishable from vehicle control at doses producing maximal GH responses — a selectivity profile not replicated by any other characterised GHRP.

Why Does Combining CJC-1295 Without DAC With Ipamorelin Produce More GH Than Either Alone?

CJC-1295 Without DAC activates GHRH-R/Gs/cAMP/PKA signalling in somatotrophs — elevating intracellular cAMP, priming secretory granules, and increasing GH gene transcription. Ipamorelin activates GHS-R1a/Gq/IP₃/calcium signalling — elevating intracellular calcium and driving secretory granule fusion and exocytosis. These two intracellular signalling axes are complementary: cAMP/PKA primes the somatotroph for secretion while IP₃/calcium triggers the exocytotic event. Co-activation of both pathways simultaneously produces convergent signal amplification — a superadditive GH release response that substantially exceeds the sum of the individual peptide responses and underlies the rationale for the dual-peptide combination format in GH axis research.

What is the Research Difference Between the CJC-1295 Without DAC + Ipamorelin and CJC-1295 Without DAC + GHRP-2 Combinations?

The primary distinction is GH selectivity. GHRP-2 is a high-potency GHS-R1a agonist that produces significant cortisol, ACTH, and prolactin co-stimulation alongside GH release — through engagement of hypothalamic CRH pathways proportional to its GHS-R1a potency. Substituting GHRP-2 for Ipamorelin in the combination produces a modestly higher peak GH response but introduces confounding HPA axis activation that complicates interpretation in studies examining GH-specific biology. The CJC-1295 Without DAC + Ipamorelin combination is preferred when clean, GH-selective axis stimulation without HPA co-activation is required; GHRP-2 combinations are used when the researcher requires maximum GH pulse amplitude and HPA co-stimulation is an acceptable or studied variable.

How Do I Reconstitute CJC-1295 Without DAC and Ipamorelin for Laboratory Use?

Reconstitute each peptide separately with sterile water or appropriate laboratory buffer by adding solvent slowly down the vial wall and swirling gently — do not vortex. Both peptides reconstitute readily in aqueous buffers without organic co-solvents. Prepare working stocks at required concentration, aliquot into single-use volumes, and store at -80°C. For combination studies, peptides may be combined at the point of use by mixing reconstituted stock solutions at the required molar ratio — co-formulation prior to lyophilisation is not required for standard research applications.

How Quickly is the Combination Delivered to Europe?

Delivery to EU and European destinations typically takes 3–7 working days via tracked international courier with packaging maintaining peptide stability throughout transit.

Product Specifications — Combination

Parameter	CJC-1295 Without DAC	Ipamorelin
Peptide Class	GHRH analogue	Synthetic GHRP — GHS-R1a agonist
Receptor Target	GHRH-R	GHS-R1a (Ghrelin Receptor)
Signalling Pathway	Gs/cAMP/PKA	Gq/IP₃/calcium
Half-life	~30 minutes	~2 hours
GH Selectivity	N/A (GHRH pathway)	Highest in GHRP class
Cortisol/Prolactin	None	Minimal
Combination Synergy	Superadditive GH release via dual-pathway somatotroph co-activation
Purity	≥99%	≥99%
Verification	HPLC & Mass Spectrometry	HPLC & Mass Spectrometry
Form	Sterile Lyophilised Powder	Sterile Lyophilised Powder
Solubility	Sterile water or laboratory buffer	Sterile water or laboratory buffer
Storage	-20°C, protected from light and moisture	-20°C, protected from light and moisture
Intended Use	Research use only	Research use only

Research Disclaimer

CJC-1295 Without DAC and Ipamorelin are supplied exclusively for legitimate scientific research conducted within licensed laboratory environments. These products are not approved for human consumption, self-administration, or any therapeutic, clinical, or veterinary application. They must be handled solely by qualified researchers in compliance with applicable EU regulations, national legislation, and institutional ethics guidelines. By purchasing, you confirm these compounds will be used exclusively for approved in vitro or pre-clinical research purposes.