Overview: Cartalax is a synthetic tripeptide bioregulator (Ala-Glu-Asp) developed from the Russian Khavinson peptide research program. Unlike most peptides that act on cell-surface receptors, Cartalax is studied for its ability to penetrate cell nuclei and bind directly to DNA, modulating gene expression patterns linked to cellular aging and connective tissue maintenance. Research has focused on chondrocyte biology, fibroblast aging, and extracellular matrix homeostasis. Key senescence-associated genes investigated include p53, p16, and SIRT-6. Studies have been conducted in fibroblast, chondrocyte, kidney cell, and mesenchymal stem cell models. Evidence base is currently preclinical — no published Phase II or III human clinical trials exist. Molecular weight: 333.29 g/mol.

Wolverine is a dual-peptide research blend combining equimolar concentrations of BPC-157 and TB-500 (Thymosin Beta-4 fragment) in a single lyophilized vial. The rationale for co-administration is mechanistic complementarity: BPC-157 primarily acts through the nitric oxide (NO) system and growth factor upregulation (VEGF, EGF) to accelerate local tissue repair, while TB-500 promotes systemic actin polymerization, cell migration, and angiogenesis via Thymosin Beta-4's Tβ4 pathway. Together, they address both local and systemic dimensions of tissue recovery. Research interest in combined peptide protocols has grown significantly, with preclinical models suggesting additive or synergistic effects on tendon, ligament, and muscle healing timelines.

Retatrutide (LY3437943) represents the next frontier in metabolic peptide research — a triple agonist simultaneously activating glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and glucagon receptors. This triple mechanism distinguishes it from semaglutide (GLP-1 only) and tirzepatide (GLP-1 + GIP), adding glucagon receptor activation to enhance energy expenditure through thermogenesis. Phase 2 clinical trial data published in the New England Journal of Medicine (2023) demonstrated remarkable efficacy: at the 12mg dose, participants achieved a mean body weight reduction of 17.5% at 24 weeks and 24.2% at 48 weeks — among the highest weight loss figures ever recorded in a pharmacological obesity trial. A separate Phase 2a study published in Nature Medicine (2024) showed retatrutide reduced liver fat by 82.4% at 24 weeks in participants with metabolic dysfunction-associated steatotic liver disease (MASLD). Retatrutide is more potent at GIPR by a factor of 8.9 compared to endogenous GIP, and is currently advancing through Phase 3 trials.

5-Amino-1-methylquinolinium (5-Amino-1MQ) is a small-molecule inhibitor of Nicotinamide N-Methyltransferase (NNMT), an enzyme highly expressed in adipose tissue that consumes S-adenosylmethionine (SAM) and produces 1-methylnicotinamide — effectively acting as a metabolic brake on NAD+ availability and fat cell energy expenditure. By blocking NNMT, 5-Amino-1MQ increases intracellular NAD+ levels, activates SIRT1 (a key longevity and metabolic regulator), and shifts adipocytes from a storage-dominant to a metabolically active state. Preclinical research has demonstrated that NNMT inhibition reduces fat mass, improves insulin sensitivity, and increases energy expenditure without stimulant-like cardiovascular effects. The compound is of particular interest in the context of obesity research because NNMT expression is elevated in obese adipose tissue, suggesting a pathological role in metabolic dysfunction.

Glutathione (GSH) is the body's most abundant endogenous antioxidant — a tripeptide (Glu-Cys-Gly) synthesized in virtually every cell and serving as the primary defense against oxidative stress, reactive oxygen species (ROS), and xenobiotic toxins. It functions as a cofactor for glutathione peroxidase (GPx) and glutathione S-transferase (GST), enzymes critical for neutralizing lipid peroxides and conjugating toxic compounds for hepatic elimination. Research has demonstrated that glutathione depletion is associated with accelerated aging, impaired immune function, neurodegenerative disease progression, and reduced detoxification capacity. Injectable glutathione bypasses the poor oral bioavailability of the intact tripeptide (which is largely degraded in the GI tract), delivering reduced GSH directly to systemic circulation. Additional research interest exists in glutathione's role in melanin regulation — reduced GSH shifts melanin synthesis toward lighter pheomelanin, which has driven investigation into its skin-brightening properties.

GHK-Cu (Glycyl-L-Histidyl-L-Lysine complexed with copper) is one of the most extensively studied peptides in dermatological and regenerative research, with a literature base spanning over four decades. Naturally present in human plasma, saliva, and urine, GHK-Cu levels decline significantly with age — from approximately 200ng/mL at age 20 to 80ng/mL by age 60. Research has demonstrated that GHK-Cu stimulates collagen, elastin, and glycosaminoglycan synthesis; activates wound healing and tissue remodeling; upregulates antioxidant gene expression (SOD, catalase); and modulates over 4,000 human genes — approximately 31% of the human genome — according to gene array studies. Hair follicle research has shown GHK-Cu increases follicle size, stimulates hair growth, and reverses miniaturization. Its copper-chelating properties also contribute to angiogenesis and nerve outgrowth. Available in 50mg and 100mg vials.

Tesamorelin is a synthetic analogue of Growth Hormone-Releasing Hormone (GHRH) consisting of the full 44-amino acid sequence of human GHRH with a trans-3-hexenoic acid group attached to stabilize it against enzymatic degradation. It is FDA-approved (as Egrifta) for the treatment of HIV-associated lipodystrophy — specifically excess visceral adipose tissue accumulation — making it one of the few peptides in the TDS catalog with a regulatory approval pathway. Tesamorelin stimulates the pituitary gland to release growth hormone in a physiological, pulsatile pattern, which in turn elevates IGF-1 levels and promotes lipolysis in visceral adipose tissue. Clinical trials demonstrated significant reductions in visceral fat (approximately 15–18% reduction vs. placebo) without the supraphysiological GH levels associated with exogenous HGH administration. Research interest extends to cognitive function, where elevated IGF-1 has been associated with improved memory and executive function in aging populations.

GHRP-6 (Growth Hormone Releasing Peptide-6) is a synthetic hexapeptide that acts as a ghrelin mimetic, binding to the growth hormone secretagogue receptor (GHSR-1a) in the pituitary and hypothalamus to stimulate robust, pulsatile growth hormone release. Unlike GHRH analogues (CJC-1295, Tesamorelin) which extend the duration of GH pulses, GHRP-6 triggers the amplitude of GH release through a complementary mechanism — making the two classes synergistic when combined. A notable characteristic of GHRP-6 is its pronounced appetite-stimulating effect, mediated through ghrelin receptor activation in the hypothalamus and gut. This property makes it of particular research interest in cachexia, muscle wasting, and recovery protocols where caloric intake is a limiting factor. GHRP-6 also demonstrates cardioprotective properties in preclinical models, independent of its GH-releasing effects.

Semax is a synthetic heptapeptide analogue of the ACTH(4-7) fragment (Met-Glu-His-Phe) with a Pro-Gly-Pro C-terminal extension that confers metabolic stability. Originally developed in Russia by the Institute of Molecular Genetics, Semax has been approved in Russia and Ukraine for the treatment of stroke, transient ischemic attacks, and cognitive impairment. Its primary mechanism involves upregulation of Brain-Derived Neurotrophic Factor (BDNF) and its receptor TrkB, as well as modulation of the serotonergic and dopaminergic systems. BDNF is the brain's primary growth factor for neuronal survival, synaptic plasticity, and long-term potentiation — the cellular basis of learning and memory. Research has also demonstrated Semax's ability to enhance stress resilience through modulation of the HPA axis, reduce neuroinflammation, and improve attention and working memory in both healthy and cognitively impaired subjects. Unlike many nootropics, Semax has a well-characterized mechanism and a meaningful clinical literature base.

Dihexa (N-hexanoic-Tyr-Ile-(6) aminohexanoic amide; PNB-0408) is a synthetic, metabolically stabilized analogue of angiotensin IV developed at Washington State University by Drs. Harding and Wright. It was designed to overcome the sub-minute serum half-life of angiotensin IV by incorporating structural modifications that confer enzymatic stability, blood-brain barrier permeability, and oral bioavailability — resulting in a serum half-life of approximately 12.7 days in rats. Dihexa's mechanism centers on augmentation of the Hepatocyte Growth Factor (HGF)/c-Met receptor signaling pathway, which promotes dendritic spine formation and synaptogenesis (the formation of new synaptic connections). Preclinical research demonstrated that Dihexa restored cognitive performance in aged rats with memory deficits at picomolar concentrations. Its prodrug Fosgonimeton was advanced into the Phase 2/3 LIFT-AD trial for Alzheimer's disease by Athira Pharma, which reported in 2024 that primary endpoints were not met — a sobering reminder of the gap between preclinical synaptogenesis data and clinical cognitive outcomes. Dihexa remains an important research tool for investigating HGF/c-Met-mediated neuroplasticity.

PT-141 (Bremelanotide) is a synthetic cyclic heptapeptide analogue of alpha-MSH that acts as an agonist at melanocortin receptors MC3R and MC4R in the central nervous system — specifically in the hypothalamus and limbic system — to directly stimulate sexual arousal pathways. Unlike PDE5 inhibitors (sildenafil, tadalafil) which act peripherally on vascular smooth muscle, PT-141 operates centrally on the neural circuits governing sexual desire and motivation, making it effective in both men and women regardless of vascular function. PT-141 received FDA approval in 2019 (as Vyleesi) for the treatment of Hypoactive Sexual Desire Disorder (HSDD) in premenopausal women — making it one of the few peptides in the TDS catalog with full FDA approval. Research has demonstrated efficacy in both male and female sexual dysfunction, with effects mediated through dopaminergic and oxytocinergic pathways downstream of MC4R activation.

Kisspeptin-10 is the bioactive C-terminal fragment of the KISS1 gene product and a potent endogenous activator of the hypothalamic-pituitary-gonadal (HPG) axis. It binds with high affinity to the kisspeptin receptor (KISS1R / GPR54), triggering a robust and sustained release of gonadotropin-releasing hormone (GnRH) from hypothalamic neurons. This GnRH pulse drives downstream secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary — the central hormonal cascade governing testosterone production, ovarian function, and reproductive signaling. Unlike direct testosterone or LH supplementation, Kisspeptin-10 operates upstream, stimulating the body's own endogenous hormonal machinery rather than bypassing it.

Thymosin Alpha-1 (Tα1) is a 28-amino acid peptide naturally secreted by the thymus gland that serves as a master regulator of T-cell maturation and immune response amplification. It is commercially available as Thymalfasin (Zadaxin) and has been approved in over 35 countries for the treatment of hepatitis B, hepatitis C, and as an adjuvant to cancer immunotherapy and vaccines. Tα1 acts through Toll-like receptor (TLR) signaling pathways to enhance dendritic cell maturation, increase natural killer (NK) cell activity, upregulate MHC class I and II expression, and promote Th1 cytokine production (IL-2, IFN-γ). Research has demonstrated efficacy in chronic viral infections, immunodeficiency states, and as a vaccine adjuvant — with a particularly strong evidence base in hepatitis and sepsis models. Its safety profile is well-established across decades of clinical use.