# KLOW Components — Per-peptide reference plates > Component sheet for the KLOW research blend: GHK-Cu, BPC-157, TB-500, and KPV — molecular weights, structures, and primary research actions per peptide. Research-only. Each KLOW component is a different molecule with a different mechanism, a different literature base, and a different regulatory posture. This sheet documents each in turn. ## G — GHK-Cu (50 mg per 80 mg vial) GHK-Cu is the copper-bound complex of glycyl-L-histidyl-L-lysine, a tripeptide first isolated from human albumin by Loren Pickart in 1973 [6]. Molecular weight is 340.4 Da for the free peptide and 403.9 Da for the copper complex. Serum GHK concentration falls from approximately 200 ng/mL at age 20 to approximately 80 ng/mL by age 60 — a quantitative decline that has anchored most of the subsequent research interest in this compound [6]. The primary research actions documented for GHK-Cu are tissue remodeling, fibroblast activation, collagen and glycosaminoglycan synthesis, metalloproteinase modulation, and broad gene-expression modulation. A 2018 Connectivity Map analysis showed that GHK reverted a 127-gene COPD-severity signature toward the healthy baseline — a striking demonstration of transcriptional reach for a tripeptide [8]. In organ culture, GHK-Cu increased hair shaft elongation and dermal papilla cell proliferation, with effects compared to 2% minoxidil in early follow-up reviews [9]. GHK-Cu is used in cosmetic formulations but has no drug approval. In research, it is typically formulated at 0.01-0.05% topical concentration; in cell culture, in the nanomolar-to-micromolar range [6]. ## B — BPC-157 (10 mg per 80 mg vial) BPC-157 — Body Protection Compound 157 — is a 15-amino-acid pentadecapeptide with the sequence GEPPPGKPADDAGLV, derived from a fragment of a protein found in human gastric juice [4]. Molecular weight is 1419.5 Da. In rat models of musculoskeletal injury, BPC-157 at 10 micrograms per kilogram intraperitoneal improved Achilles tendon-to-bone healing and reversed corticosteroid-induced healing impairment [1]. The same dose accelerated healing of transected rat Achilles tendon and stimulated tendocyte growth in vitro [4]. In rats with disabled myotendinous junctions, 10 ug/kg ip or per-oral exposure recovered junction architecture and functional output [23]. Mechanistically, BPC-157 activates the VEGFR2-Akt-eNOS angiogenic pathway, increasing vessel density and accelerating blood flow recovery in ischemic rat hindlimb [2], and modulates vasomotor tone via Src-Caveolin-1-eNOS signaling in isolated aortic rings [3]. A 2023 review documents BPC-157 effects across multiple rodent models of brain-gut and gut-brain axis dysfunction [17]. The human evidence is sparse. A single Phase II trial of PL 14736 (BPC-157 enema) in mild-to-moderate ulcerative colitis was advanced by Pliva (Croatia); the results were never published in peer-reviewed literature [5]. The 2025 HSS Journal systematic review found 36 included articles, of which 35 were preclinical and only one was a retrospective clinical case series [19]. BPC-157 is prohibited under WADA category S0. ## T — TB-500 / Thymosin Beta-4 (10 mg per 80 mg vial) TB-500 is the vendor name for synthetic thymosin beta-4, a 44-amino-acid peptide with molecular weight 4963 Da. The active mechanism is G-actin sequestration via the LKKTET binding motif — by binding monomeric actin, thymosin beta-4 regulates cytoskeletal dynamics needed for cell migration and tissue remodeling [10]. In preclinical wound models, thymosin beta-4 accelerated re-epithelialization, organized connective tissue, and prevented myofibroblast differentiation, reducing scar formation in rat incisional wounds [11]. In a Phase 2 trial of patients with stasis and pressure ulcers who did heal, topical thymosin beta-4 accelerated healing by approximately one month [10]. In healthy human volunteers, single intravenous doses from 42 mg to 1260 mg and multiple-dose 14-day regimens produced no serious adverse events [12]. The most clinically advanced TB-500 work outside ophthalmology is cardiac: a 2025 study reported that IV thymosin beta-4 at 0.5 ug/kg and 1.0 ug/kg, given within 12 hours of PCI in STEMI patients, reduced infarct size and improved left-ventricular function vs placebo at 90-day follow-up [18]. Ophthalmic RGN-259 (0.1% thymosin beta-4 solution) met its primary endpoint in a US Phase 3 trial in neurotrophic keratopathy [13]; the parallel European SEER-3 trial missed its endpoint, attributed to placebo-arm response. TB-500 is prohibited under WADA category S0. ## K — KPV (10 mg per 80 mg vial) KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone — H-Lys-Pro-Val-OH, molecular weight 342.4 Da, corresponding to residues 11-13 of alpha-MSH [14,16]. Unlike the parent hormone, KPV does not bind melanocortin receptors. Its anti-inflammatory activity proceeds through PepT1-mediated cellular uptake and NF-kB pathway suppression [14]. In the canonical Dalmasso 2008 study, KPV at 100 micromolar in drinking water reduced inflammation markers by approximately 50% in murine DSS and TNBS colitis, with proportionate reductions in TNF-alpha, IL-1-beta, and IL-6 [14]. In a follow-up AOM/DSS colitis-associated cancer model, oral KPV reduced tumor count and dysplasia [15]. The selective delivery is partly explained by PepT1 upregulation in inflamed colonic tissue — KPV accumulates preferentially at the disease site. In cell culture, alpha-MSH-related peptides including KPV reduce NF-kB nuclear translocation and lower TNF-alpha and IL-1-beta secretion in human and murine immune cells [16]. KPV has no published human clinical trial data and is scheduled for FDA Pharmacy Compounding Advisory Committee review in mid-2026. --- A technical reference set for the peer-reviewed literature — not a clinic, not a vendor, not a prescription.