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Free U.S. shipping on orders over $150Tesamorelin, CJC-1295 No DAC, and ipamorelin are a combination of investigational peptides that engage complementary growth hormone–releasing hormone (GHRH) and ghrelin receptor (GHS) pathways to modulate endogenous growth hormone pulsatility.
Mechanistic studies support GHRH–GHS cross-talk, though direct clinical evaluation of this three-peptide combination remains limited.
Tesamorelin is a synthetic analog of growth hormone–releasing hormone (GHRH) consisting of 44 amino acids, designed to stimulate endogenous growth hormone (GH) secretion from the anterior pituitary.
By activating the GHRH receptor, tesamorelin promotes pulsatile GH release and downstream increases in insulin-like growth factor-1 (IGF-1), while preserving physiologic feedback regulation.
Tesamorelin has been studied in metabolic research contexts for its ability to metabolize fat while maintaining muscle mass, particularly in HIV patients [1].
CJC-1295 is a synthetic peptide analog of growth hormone–releasing hormone that retains the core bioactive sequence of native GHRH but lacks the drug affinity complex (DAC) modification.
As a result, it has a shorter functional half-life and more closely mimics physiologic, pulsatile GH signaling rather than sustained elevation.
By binding to the GHRH receptor on pituitary somatotrophs, CJC-1295 without DAC stimulates endogenous growth hormone release and downstream IGF-1 production in a natural and feedback-regulated manner [2].
In research settings, it is often used as a tool to engage the GHRH axis without prolonged GH exposure.
Ipamorelin is a synthetic pentapeptide growth hormone secretagogue that selectively activates the ghrelin (GHS-R1a) receptor in the hypothalamus and pituitary.
Through this pathway, ipamorelin promotes pulsatile growth hormone release without significantly stimulating other pituitary hormones such as cortisol or prolactin [3].
In research models, ipamorelin is a commonly studied complement to GHRH analogs when examining coordinated regulation of the somatotropic axis.
This three-peptide combination is best understood as a multi-node strategy to engage the somatotropic axis.
Two components, tesamorelin and CJC-1295 No DAC, are GHRH-pathway agonists, while ipamorelin activates the ghrelin/GHS-R1a pathway, a distinct control system that can amplify GH release through complementary signaling.
Both tesamorelin and CJC-1295 without DAC stimulate the GHRH receptor on pituitary somatotrophs, via adenylyl cyclase activation and increased cAMP, supporting physiologic GH pulse generation when pituitary function is intact.
The most evidence-supported synergy in this stack comes from combining GHRH receptor activation (tesamorelin/CJC-1295 without DAC) with GHS-R1a activation (ipamorelin).
GHS compounds and ghrelin receptor agonism stimulate GH release via signaling that is typically described as PLC/second-messenger (Ca²⁺/DAG)–linked, distinct from the cAMP-centric GHRH pathway [4].
Controlled mechanistic studies show that co-activation of the GHRH receptor and the GHS receptor can amplify intracellular signaling beyond either pathway alone.
In a receptor-defined cell system expressing both receptors, activation of a GHS pathway (including ghrelin) potentiated the cAMP response to GHRH. The cAMP response approximately doubled compared with GHRH alone, suggesting receptor-level cross-talk that enhances somatotroph responsiveness [5].
This type of finding provides a strong rationale for pairing a GHRH analog with a selective GH secretagogue like ipamorelin when the goal is to model enhanced pulsatile GH dynamics rather than sustained GH elevation.
Aside from muscle anabolism, CJC-1295 combined with ipamorelin may also activate chondrocytes and osteoblast differentiation, suggesting potential use for cartilage and bone regeneration [6].
Direct studies evaluating tesamorelin + CJC-1295 No DAC + ipamorelin as a three-agent combination are not well represented in the peer-reviewed literature. What does exist is:
Given this, the most defensible conclusion is that the triple stack is mechanistically plausible, but not yet validated as a combined regimen in controlled clinical trials.
At a conceptual level, allocating more total mass to the GHRH-analog component (e.g., tesamorelin 6 mg alongside lower-dose CJC-1295 No DAC and ipamorelin) can be interpreted as emphasizing primary drive through the traditional GHRH pathway, with ipamorelin positioned as a complementary amplifier via GHS-R1a cross-talk.
Beyond that general framework, the optimal ratio is not established in public evidence and should be treated as an empirical design choice rather than a settled standard.
References:
1 Adrian, S., Scherzinger, A., Sanyal, A., Lake, J. E., Falutz, J., Dubé, M. P., et al. (2019) The growth hormone releasing hormone analogue, tesamorelin, decreases muscle fat and increases muscle area in adults with HIV. J. Frailty Aging, SERDI 8, 154–159
2 Teichman, S. L., Neale, A., Lawrence, B., Gagnon, C., Castaigne, J.-P. and Frohman, L. A. (2006) Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J. Clin. Endocrinol. Metab. 91, 799–805
3 Raun, K., Hansen, B. S., Johansen, N. L., Thøgersen, H., Madsen, K., Ankersen, M., et al. (1998) Ipamorelin, the first selective growth hormone secretagogue. Eur. J. Endocrinol., Oxford University Press (OUP) 139, 552–561
4 Akalu, Y., Molla, M. D., Dessie, G. and Ayelign, B. (2020) Physiological effect of ghrelin on body systems. Int. J. Endocrinol., John Wiley & Sons, Ltd 2020, 1385138
5 Cunha, S. R. and Mayo, K. E. (2002) Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3’,5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology, The Endocrine Society 143, 4570–4582
6 Rahman, O. F., Lee, S. J. and Seeds, W. A. (2026) Therapeutic peptides in orthopaedics: Applications, challenges, and future directions. J. Am. Acad. Orthop. Surg. Glob. Res. Rev., Ovid Technologies (Wolters Kluwer Health) 10, e25.00236
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Tesamorelin + CJC-1295 (No DAC)+ Ipamorelin is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders are processed within 1–3 business days after payment confirmation. Orders placed after 3:00 PM Pacific time or on weekends and holidays will begin processing the next business day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
Character Snapshot In combination, tesamorelin and ipamorelin represent a dual-pathway approach to modulating endogenous GH pulsatility, leveraging established physiological interactions between GHRH and ghrelin signaling. While direct combination studies are limited, existing mechanistic and translational evidence supports further investigation of this pairing as a research model for coordinated GH axis regulation. Tesamorelin Tesamorelin is a synthetic analog of growth hormone–releasing hormone (GHRH) composed of 44 amino acids, designed to stimulate endogenous, pulsatile growth hormone (GH) secretion from the anterior pituitary [1]. By binding to the GHRH receptor, tesamorelin activates cAMP-mediated signaling in somatotroph cells, promoting downstream increases in insulin-like growth factor-1 (IGF-1) while preserving normal feedback regulation [2]. Tesamorelin is a well-characterized tool for elucidating GHRH-driven regulation as both model organisms and clinical research have investigated for effects on [3]: GH axis modulation Lipid metabolism Visceral adipose tissue Ipamorelin Ipamorelin is a synthetic pentapeptide growth hormone secretagogue that selectively activates the ghrelin (GHS-R1a) receptor in the hypothalamus and pituitary [4]. Through this pathway, ipamorelin stimulates pulsatile growth hormone (GH) release without significantly increasing other pituitary hormones such as cortisol or prolactin. In research settings, ipamorelin has been investigated for its high signaling specificity and favorable endocrine selectivity, making it a complementary agent to GHRH analogs when studying coordinated regulation of endogenous GH secretion. Synergy The rationale for combining tesamorelin and ipamorelin is grounded in well-characterized physiological cross-talk between the GHRH and ghrelin/GHS signaling systems, which regulate the amplitude and timing of endogenous growth hormone (GH) pulses. Rather than acting redundantly, these peptides engage distinct but convergent control pathways within the somatotropic axis. Complementary mechanisms of action Tesamorelin is a GHRH analog that activates the GHRH receptor on pituitary somatotrophs, while Ipamorelin is a selective ghrelin (GHS-R1a) receptor agonist. GHS-R1a activation is typically associated with PLC-linked signaling, intracellular calcium mobilization, and enhanced somatotroph responsiveness [5]. Importantly, ghrelin/GHS signaling does not independently raise cAMP, but it can potentiate GHRH-driven cAMP responses when both receptors are engaged. An in vivo study examined whether ghrelin exhibited synergistic effects with growth hormone–releasing hormone (GHRH) on growth hormone (GH) secretion [6]. Normal adult male participants were given an intravenous administration of ghrelin at varying doses (0.08, 0.2, and 1.0 μg/kg), either alone or in combination with GHRH (1.0 μg/kg). Results showed that: At lower ghrelin doses (0.08 and 0.2 μg/kg), combined administration with GHRH resulted in a statistically significant synergistic increase in GH secretion (p < 0.05). At the higher, equivalent ghrelin dose (1.0 μg/kg), a similar trend toward synergy was observed, but with no statistical significance. No synergistic effects were observed for ACTH or prolactin, indicating pathway specificity for GH secretion. These findings demonstrate a selective and dose-dependent synergistic interaction between ghrelin and GHRH in stimulating GH release in humans. The absence of synergy for other pituitary hormones suggests that the interaction is specific to the somatotropic axis, rather than generalized pituitary activation. Direct clinical trials specifically evaluating tesamorelin combined with ipamorelin are limited. However, the broader literature provides several relevant lines of evidence: Cell-based and animal studies demonstrate synergistic GH release when GHRH and ghrelin or GHS compounds are co-administered, relative to either pathway alone [7,8]. Clinical and translational research on tesamorelin shows robust stimulation of pulsatile GH and downstream IGF-1 in populations with intact pituitary function [9,3]. Human pharmacology studies of GHS compounds, including ipamorelin-class peptides, illustrate selective GH release with minimal off-target pituitary hormone activation [6]. Taken together, this data supports the potential of tesamorelin–ipamorelin synergy via coordinated engagement of complementary regulatory pathways, even though formal combination trials remain sparse. Dosing From a research-design perspective, allocating a greater proportion of the total peptide mass to tesamorelin (7 mg) can be viewed as emphasizing primary drivers through the main GHRH pathway, which establishes pulse timing and baseline GH output. Ipamorelin (3 mg) can then function as a selective amplifier, enhancing somatotroph responsiveness through GHS-R1a–mediated cross-talk without broadly activating appetite or stress-related endocrine pathways. This lower ghrelin receptor agonist to GHRH ratio is in agreement with the literature in terms of producing synergistic GH secretion effects [6]. Beyond this high-level rationale, optimal dosing ratios are not established in the open literature and should be regarded as empirical parameters rather than evidence-based standards. References: 1 (2012) Bremelanotide. In LiverTox: Clinical and Research Information on Drug-Induced Liver Injury, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda (MD) 2 Halmos, G., Szabo, Z., Dobos, N., Juhasz, E. and Schally, A. V. (2025) Growth hormone-releasing hormone receptor (GHRH-R) and its signaling. Rev. Endocr. Metab. Disord., Springer Science and Business Media LLC 26, 343–352 3 Results from the 26-week Confirmatory, Phase 3 Trial of Tesamorelin (TH9507), a Growth Hormone-Releasing Factor Analogue, in HIV Patients with Excess Abdominal Fat: A Multicenter, Double-blind, Placebo-controlled Study with 404 Randomized Patients https://www.natap.org/2008/IAS/IAS_56.htm 4 Sinha, D. K., Balasubramanian, A., Tatem, A. J., Rivera-Mirabal, J., Yu, J., Kovac, J., et al. (2020) Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl. Androl. Urol., AME Publishing Company 9, S149–S159 5 Mear, Y., Enjalbert, A. and Thirion, S. (2013) GHS-R1a constitutive activity and its physiological relevance. Front. Neurosci., Frontiers Media SA 7, 87 6 Hataya, Y., Akamizu, T., Takaya, K., Kanamoto, N., Ariyasu, H., Saijo, M., et al. (2001) A low dose of ghrelin stimulates growth hormone (GH) release synergistically with GH-releasing hormone in humans. J. Clin. Endocrinol. Metab., The Endocrine Society 86, 4552 7 Cunha, S. R. and Mayo, K. E. (2002) Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3’,5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology, The Endocrine Society 143, 4570–4582 8 Casanueva, F. F. and Dieguez, C. (1999) Growth hormone secretagogues: Physiological role and clinical utility. Trends Endocrinol. Metab., Elsevier BV 10, 30–38 9 Stanley, T. L., Chen, C. Y., Branch, K. L., Makimura, H. and Grinspoon, S. K. (2011) Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. J. Clin. Endocrinol. Metab., The Endocrine Society 96, 150–158
Snapshot: Thymalin is a polypeptide isolated from the thymus gland and has been studied for its role in supporting immune function. Research suggests it has a role in influencing T-cell activity, cytokine modulation, oxidative defense, aging processes, and cellular resilience. What Is Thymalin? Thymalin is a polypeptide, naturally derived and isolated from the thymus gland [1]. Endogenous Thymalin naturally declines with age, paralleling thymic involution and reduced immune efficiency. It consists of short peptides, typically 2–8 amino acids in length, that support gene expression in immune and hematopoietic cells [1]. The dipeptide L-Glu-L-Trp, often referred to as the EW peptide, is the bioactive fragment with the most notable immunoregulatory properties [2]. Research demonstrates it can influence cytokine production, enhance communication between immune cells, and contribute to a healthier immune system responsiveness [2]. Because it can act at low concentrations, it has become a promising candidate in targeted immunomodulation strategies [1]. Although often confused with Thymulin, Thymalin is a polypeptide extract, while Thymulin is a zinc-dependent non-peptide hormone [1, 3]. Thymalin is thought to regulate thymic activity more broadly than Thymulin, which appears to enhance specific thymic hormone functions [1, 4]. Thymalin Peptide Benefits Thymalin is clinically studied as a potential molecule that supports immune balance, antioxidant defenses, and tissue repair processes and promotes healthy cellular aging through multiple biologically active pathways. Immunomodulation Thymalin supports immune function by promoting T-cell differentiation, improving cytokine signaling, and enhancing lymphocyte activity [1]. In hematopoietic stem cells, it reduced the expression of CD44 and CD117, which are molecules associated with early stem cell proliferation and maintenance. This indicated a shift toward the development of mature immune cells [1]. These cell also had significant increases in CD28 expression, found on CD4+ and CD8+ T-lymphocytes, critical for T-cell activation and viral immunity [1]. In a comparative study, Thymalin significantly improved immune cell counts in those with respiratory viral infection, whereas standard therapy had minimal effects [5]. It increased total leukocyte counts by 25% and lymphocytes by 92%, despite lower baseline lymphocyte counts compared to controls [5]. Monocytes measured in blood rose by 55% with Thymalin compared to 42% on standard therapy, and eosinophils increased 4.6-fold versus 3.1-fold, respectively [5]. Thymalin also enhanced adaptive and innate immunity, raising T- and B-lymphocytes and NK cells by 2–2.4 times and boosting CD4+, CD8+, and CD3+HLA-DR+ cells by 2.2–3.4 times. In contrast, standard treatment including antiviral, antibiotics, and oxygen had no significant impact [5]. These findings suggest Thymalin has a role in restoring immune competence in conditions where immunity may be compromised. Anti-Inflammatory and Regenerative Benefits Thymalin has demonstrated broad anti-inflammatory and regenerative potential. Its short peptide composition, particularly EW and KE dipeptides, can penetrate the cell nucleus and bind to specific DNA and histone regions [6]. This capability modulates gene expression involved in cytokine production, antioxidant defense, and tissue repair processes [5]. Molecular modeling shows that the EW and KE peptides interact with DNA regions that regulate key inflammatory genes, including ACE2, CYSLTR1, and CHUK – proteins deeply involved in driving cytokine-storm responses during severe viral infections [2]. In cell-based studies in a human mononuclear cell model of LPS-induced inflammation, Thymalin and its dipeptides reduced IL-1β, IL-6, and TNF-α by 1.4–6-fold, showing a direct capacity to downregulate pro-inflammatory cytokine synthesis [2]. Beyond acute immune modulation, thymalin may reduce oxidative stress, stabilize cyclic nucleotide balance, enhance neutrophil chemotaxis and phagocytosis, and support tissue regeneration [7]. Studies in various pathological models show reduced apoptosis and improved metabolic markers, suggesting that Thymalin helps restore cellular homeostasis and promotes recovery across multiple organ systems [7]. Geroprotective Benefits Thymalin has been widely investigated for its geroprotective potential. Long-term studies in aging models show promising effects across multiple physiological systems, with potential to preserve cardiovascular, neurological, and metabolic function while reducing chronic, low-grade inflammation which is one of the major contributors to biological aging [4]. It appears to promote greater resilience and functional stability as the body ages, supporting T-cell production, normalizing cytokine activity, and influencing key regulatory pathways involved in immune and endocrine balance [4]. In one study spanning up to 8 years involving 266 older adults, researchers found Thymalin – either alone or combined with a pineal peptide – helped to normalize core physiological functions, including cardiovascular, endocrine, neurological, and metabolic markers [8]. Those receiving peptide therapy experienced a 2–2.4-fold reduction in acute respiratory infections, fewer cardiovascular complications, and improved bone health and had significantly lower mortality [8]. References 1 Khavinson, V. K., Linkova, N. S., Kvetnoy, I. M., Polyakova, V. O., Drobintseva, A. O., Kvetnaia, T. V., et al. (2020) Thymalin: Activation of Differentiation of Human Hematopoietic Stem Cells. Bull. Exp. Biol. Med. 170, 118–122 https://doi.org/10.1007/s10517-020-05016-z 2 Linkova, N., Khavinson, V., Diatlova, A., Petukhov, M., Vladimirova, E., Sukhareva, M., et al. (2023) The influence of KE and EW dipeptides in the composition of the Thymalin drug on gene expression and protein synthesis involved in the pathogenesis of a respiratory infection. Int. J. Mol. Sci., MDPI AG 24, 13377 https://doi.org/10.3390/ijms241713377 3 Reggiani, P. C., Schwerdt, J. I., Console, G. M., Roggero, E. A., Dardenne, M. and Goya, R. G. (2014) Physiology and therapeutic potential of the thymic peptide thymulin. Curr. Pharm. Des., Curr Pharm Des 20, 4690–4696 https://doi.org/10.2174/1381612820666140130211157 4 Reggiani, P. C., Schwerdt, J. I., Console, G. M., Roggero, E. A., Dardenne, M. and Goya, R. G. (2014) Physiology and therapeutic potential of the thymic peptide thymulin. Curr. Pharm. Des. 20, 4690–4696 https://doi.org/10.2174/1381612820666140130211157 5 Kuznik, B., Khavinson, V., Shapovalov, K., Linkova, N., Lukyanov, S., Smolyakov, Y., et al. (2021) Peptide drug thymalin regulates immune status in severe older patients. Adv. Gerontol., Pleiades Publishing Ltd 11, 368–376 https://doi.org/10.1134/s2079057021040068 6 Khavinson, V. K., Linkova, N. S., Chalisova, N. I. and Ivko, O. M. (2021) The use of thymalin for immunocorrection and molecular aspects of biological activity. Biol. Bull. Rev., Pleiades Publishing Ltd 11, 377–382 https://doi.org/10.1134/s2079086421040046 7 Avolio, F., Martinotti, S., Khavinson, V. K., Esposito, J. E., Giambuzzi, G., Marino, A., et al. (2022) Peptides regulating proliferative activity and inflammatory pathways in the monocyte/macrophage THP-1 cell line. Int. J. Mol. Sci., MDPI AG 23, 3607 https://doi.org/10.3390/ijms23073607 8 Khavinson, V. K. and Morozov, V. G. (2002) Geroprotective effect of thymalin and epithalamin. Adv. Gerontol., Adv Gerontol 10, 74–84
