Research Compound Comparison Tables 2026

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Research Compound Comparison Tables 2026 — Condor Research


Condor Research · Scientific Desk
Research Use Only

Research Compound
Comparison Tables 2026

A consolidated, print-ready reference consolidating the side-by-side specifications and
evidence-quality assessments from Condor Research comparison articles. Each table
links to the full article; each data point is sourced from peer-reviewed literature
cited on that page.

Published: 2026
Source: condorresearch.com/research/
Contact: info@condorresearch.com
Supplier: Atrio Sciences s.r.o., Nitra (SK)

Research Use Only (RUO). All compounds referenced in this document are
supplied exclusively for qualified laboratory research — in vitro, cell-culture, and
controlled animal-model work — by Atrio Sciences s.r.o. (IČO 57 669 651), trading as
Condor Research. Nothing in this document constitutes a dose, a treatment protocol, a
therapeutic claim, or guidance for human or veterinary administration. Purity
characterisation (≥99% HPLC / mass spectrometry, independent third-party batch testing,
Czech Republic) applies to the supplied reference material, not to any end-use context.
All mechanisms described are derived from in vitro and/or animal literature; they do not
establish safety or efficacy in humans.

Pair 01
BPC-157 vs TB-500

Two of the most-studied tissue-repair peptides in preclinical research — chemically
unrelated, mechanistically complementary. BPC-157 is a 15-aa gastric pentadecapeptide;
TB-500 (as supplied by Condor Research) is full-length thymosin β4, a 43-aa
actin-sequestering protein.

Full article:

BPC-157 vs TB-500: A Research-Use Comparison

· References 1–9

Attribute BPC-157 TB-500 (full-length Tβ4)
Chemical class Synthetic pentadecapeptide (15 aa, gastric-sequence derived) Full-length thymosin β4 (43 aa, actin-sequestering protein)
CAS / sequence 137525-51-0 · Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val 77591-33-4 · 43-amino-acid full-length Tβ4
Primary mechanism studied (preclinical) Cytoprotection; FAK–paxillin-mediated fibroblast migration; angiogenic/vascular endpoints; GH-receptor upregulation in tendon fibroblasts1,4 G-actin sequestration; cytoskeletal remodelling; cell migration; angiogenesis via defined actin-binding motif7,9
Main preclinical research contexts Tendon, ligament, muscle, GI, vascular models2,3,5 Wound healing, corneal/dermal repair, cardiac and cell-migration models8,9
Format (Condor Research) 10 mg lyophilised vial · also available as BPC-157 Arginate Capsules 10 mg lyophilised vial · also TB-500 Capsules
Co-formulated blend BPC-157 + TB-500 (10 mg each); also in GLOW and KLOW blends
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical only
Mostly rodent / in vitro; no robust human RCTs; not an approved drug		 Preclinical only
Mostly rodent / in vitro; thymosin β4 in some early clinical contexts; Tβ4 as RUO material lacks human efficacy data
How to choose Connective-tissue repair, fibroblast behaviour, GI/vascular cytoprotection models Actin dynamics, cell migration, angiogenesis, epithelial repair models
Matched on format and ≥99% HPLC purity; differentiated by chemical class, molecular size, and the research-model literature each peptide is primarily studied within.

Pair 02
GHK-Cu vs AHK-Cu

Two copper-binding tripeptides separated by a single N-terminal residue substitution
(Gly→Ala). GHK-Cu carries nearly five decades of preclinical literature; AHK-Cu is
studied in a narrow set of in vitro and ex vivo models. Same histidine-anchored copper
pocket; very different weight of evidence.

Full article:

GHK-Cu vs AHK-Cu: A Research-Use Comparison of Two Copper-Binding Tripeptides

· References 10–17

Attribute GHK-Cu AHK-Cu
Chemical class Copper(II) tripeptide complex Copper(II) tripeptide complex
Sequence Gly-His-Lys · Cu²⁺ Ala-His-Lys · Cu²⁺
CAS 49557-75-7 682809-81-0
Molecular formula / MW C₁₄H₂₄CuN₆O₄ · 403.92 g/mol C₁₅H₂₄ClCuN₆O₄ · 451.39 g/mol
Appearance Blue-green lyophilised powder Blue lyophilised powder
Primary mechanism studied (preclinical) Copper delivery; matrix remodelling gene-expression models; cell signalling11,12; Cu(II) binding thermodynamics well-characterised13 Hair-follicle and osteogenic in vitro models14,15; coordination geometry studied in related Ala-His-His scaffold (family context, not direct evidence)16
Depth of literature Extensive — decades, hundreds of papers; first identified 197710 Limited — small number of in vitro/ex vivo studies
Format (Condor Research) 50 mg/vial · GHK-Cu Capsules 100 mg/vial · AHK-Cu Capsules
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical only
Rich preclinical corpus; limited randomised clinical data; not an approved drug in RUO context		 Preclinical only
Thin direct evidence; much inferred from related scaffolds; no clinical data
How to choose Most-characterised copper-delivery peptide; comparative reference standard N-terminal residue / coordination-geometry comparative chemistry; hair-follicle models
GHK-Cu carries a far larger and older preclinical literature. AHK-Cu is primarily studied as a structural analogue for comparative chemistry or in narrow follicle-model contexts. Both supplied at ≥99% HPLC purity with COA.

Pair 03
Ipamorelin vs CJC-1295 (no DAC)

Two GH-axis secretagogues acting through different receptors. Ipamorelin is a selective
GHS-R1a (ghrelin-receptor) pentapeptide agonist; CJC-1295 (no DAC / Modified GRF 1-29)
is a GHRH-receptor analogue. Often studied in parallel because the receptor-level
distinction is precisely the research question.

Full article:

Ipamorelin vs CJC-1295: Two Routes Into the Growth-Hormone Axis

· References 18–25

Attribute Ipamorelin CJC-1295 (no DAC)
Chemical class Pentapeptide GHS-R1a agonist (ghrelin mimetic) GHRH-receptor analogue (Modified GRF 1-29); CAS 863288-34-0
Sequence Aib-His-D-2-Nal-D-Phe-Lys-NH₂ Modified GRF(1-29) with D-Ala² substitution
Receptor target GHS-R1a (ghrelin receptor) — pituitary18 GHRH receptor — pituitary21
Key selectivity feature Does not significantly release cortisol, ACTH, or prolactin at studied doses18 Lacks DAC albumin-binding group; shorter circulating half-life than CJC-1295 DAC21
Primary mechanism studied (preclinical) GHS-R1a activation → GH pulse; GI motility models (rodent postoperative ileus)20 GHRH-R activation → GH/IGF-1 axis; pulsatility preservation; GH-knockout rescue23,25
Human data available? Pharmacokinetic and limited PD work; no robust human efficacy RCTs19 Small human studies report GH/IGF-1 responses and preserved pulsatility22,23 — not a drug approval basis
Format (Condor Research) 10 mg lyophilised vial 10 mg lyophilised vial
Co-formulated blend CJC-1295 no DAC + Ipamorelin (10 mg each)
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
WADA status Prohibited in-competition as GH secretagogue (S2) Prohibited in-competition as GH secretagogue (S2)
Evidence quality Predominantly preclinical
Pharmacokinetics described; no approved-drug status		 Early human data
Small human GH/IGF-1 studies; not approved as a drug; extrapolation to clinical efficacy unsupported
How to choose GHS-R1a biology; selective ghrelin-receptor agonism; GI motility models GHRH-receptor biology; pulsatility questions; GH/IGF-1 axis pharmacology
Different receptors, complementary axis — which is why they appear together in co-formulated blends. The research choice follows the receptor target, not a potency ranking.

Pair 04
Selank vs Semax

Two Russian regulatory-lineage neuropeptides with a shared BDNF/neurotrophin signal in
some models, but distinct parent sequences and the preclinical mechanisms primarily
studied diverge: Selank (tuftsin analogue) into GABAergic / anxiolytic models; Semax
(ACTH(4-10) analogue) into neuroprotection and cognitive models.

Full article:

Selank vs Semax: A Research-Use Comparison of Two Russian Regulatory Neuropeptides

· References 26–35

Attribute Selank Semax
Chemical class Synthetic heptapeptide analogue of tuftsin (Thr-Lys-Pro-Arg-Pro-Gly-Pro) Synthetic hexapeptide analogue of ACTH(4-10) (Met-Glu-His-Phe-Pro-Gly-Pro)
Parent / origin Tuftsin (immunopeptide Thr-Lys-Pro-Arg) + stabilising Pro-Gly-Pro extension ACTH(4-10) core with C-terminal Pro-Gly-Pro extension for stability
Primary mechanism studied (preclinical) GABAergic modulation27; anxiolytic effects in animal models26,28,29; BDNF interaction in hippocampus28 Neuroprotection in cerebral ischaemia models35; BDNF/neurotrophin modulation; anti-depressant-like effects in chronic stress models33; Aβ aggregation interference (in vitro)31
Regulatory status (Russia) Registered anxiolytic in Russia Registered nootropic / neuroprotectant in Russia
Shared model overlap Both studied using functional connectomic approaches in the same paper34; some BDNF pathway overlap in rodent work
Co-formulated blend Semax + Selank (combination vial)
Format (Condor Research) Vial (lyophilised) Vial (lyophilised)
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical + limited clinical
Rodent models; one small Russian anxiolytic trial30; not approved outside Russia in RUO context		 Preclinical + limited clinical
Rodent neuroprotection; small Russian stroke study35; not approved outside Russia in RUO context
How to choose GABAergic / anxiety / stress-model biology Neuroprotection / cognitive / ischaemia-model biology
Both carry a Russian regulatory lineage not recognised by EMA/FDA. All human observations cited above are from small, non-randomised or Russian-only studies and do not establish EMA/FDA-standard efficacy.

Pair 05
NMN vs NAD+

One enzymatic step apart on the same salvage pathway: NMN is the mononucleotide
precursor; NAD+ is the finished dinucleotide coenzyme. The research choice follows
where in the pathway the experiment needs to intervene, not which molecule is
intrinsically superior.

Full article:

NMN vs NAD+: A Research-Use Comparison of NAD Metabolism Precursors

· References 36–45

Attribute NMN Capsules NAD+
Chemical class Mononucleotide — NAD+ precursor (salvage pathway substrate) Dinucleotide — redox coenzyme and signalling substrate
Full name / CAS β-Nicotinamide mononucleotide · 1094-61-7 Nicotinamide adenine dinucleotide · 53-84-9
Molecular formula C₁₁H₁₆N₂O₈P C₂₁H₂₇N₇O₁₄P₂
Pathway position Substrate — one NMNAT-catalysed adenylylation upstream of NAD+36 Product — central redox coenzyme and sirtuin/CD38/PARP substrate36,37
Primary mechanism studied (preclinical) Precursor supplementation → NAD+ pool elevation; SIRT/PARP activation; metabolic and mitochondrial endpoints in aged rodents38,39 Redox electron transfer; direct sirtuin/CD38 substrate; mitochondrial function; age-related NAD+ decline models37
Notable human data Single-dose tolerability and metabolite changes43; one RCT in prediabetic women: increased muscle insulin sensitivity42; systematic review: physical performance not statistically significant44 Less direct human supplementation literature in RUO context; NAD+ precursor class reviewed in Nat Metab 202545
Format (Condor Research) 60 HPMC (vegan) capsules · 500 mg each 1,000 mg/vial · white lyophilised powder
Handling Capsule — no reconstitution required Reconstitute with sterile water for solution-based bench work
Purity / QC ≥99% HPLC; COA available ≥99% HPLC; third-party tested; COA
Evidence quality Early human data (inconsistent)
Rich rodent mechanism; promising but unsettled early human dataset		 Predominantly preclinical
Strong cell/biochemistry base; limited direct human supplementation RCTs in RUO context
How to choose Oral-availability / pharmacokinetic animal models; precursor-leverage questions Bench reconstitution; enzyme assays requiring intact coenzyme; direct NAD+-delivery models
Format follows function: capsules for ingestion-route animal models, lyophilised vial for bench reconstitution. The human evidence base for both is early and unsettled — the honest reading is that the preclinical signal has not been matched by a settled clinical picture.

Pair 06
Epitalon vs Pinealon

Two short Khavinson-class peptide bioregulators from the pineal lineage. Epitalon
(AEDG, tetrapeptide) is studied mainly in telomere, pineal-ageing, and lifespan models.
Pinealon (EDR, tripeptide) is investigated for neuronal antioxidant and gene-expression
endpoints. Both share a Russian research origin with limited independent replication.

Full article:

Epitalon vs Pinealon: A Research-Use Comparison of Two Khavinson Bioregulator Peptides

· References 46–53

Attribute Epitalon Pinealon
Chemical class Synthetic tetrapeptide (AEDG) — Ala-Glu-Asp-Gly Synthetic tripeptide (EDR) — Glu-Asp-Arg
Khavinson class “Cytogen” / pineal bioregulator — telomere-focused46,48 “Cytogen” / pineal bioregulator — neuro-antioxidant and gene-expression focused50,51
Primary mechanism studied (preclinical) Telomerase activation and telomere elongation in human somatic cells (in vitro)46; reduced tumour incidence and extended lifespan in rodent models48; pineal-ageing marker modulation47,49 Increased cell viability; suppression of free radical levels in vitro50; gene-expression regulation in Alzheimer’s-related models51; neuroprotective endpoints alongside structurally related EDR-class peptides52; prenatal neuroprotection in rat offspring53
Replication / independence note Primarily Khavinson-group publications; limited independent replication Primarily Khavinson-group publications; very few independent replications
Format (Condor Research) Vial (lyophilised) · Epitalon Capsules Vial (lyophilised) · Pinealon Capsules
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical only
Cell / rodent work; single-group provenance; not an approved drug; no human RCTs		 Preclinical only
Cell / rodent work; single-group provenance; not an approved drug; no human RCTs
How to choose Telomerase / telomere-length biology; lifespan-biomarker models Neuronal antioxidant / gene-expression models; EDR-class peptide biology
Single-group provenance (Khavinson et al.) is the primary caveat for both peptides. The mechanisms are plausible but require broader independent replication. For laboratory research use only.

Pair 07
5-Amino-1MQ vs SLU-PP-332

Two unrelated metabolic-research tool compounds that converge on exercise-mimetic and
NAD+-related biology by entirely different mechanisms: 5-Amino-1MQ inhibits NNMT (a
methyltransferase regulating NAD+ and methyl donors); SLU-PP-332 agonises ERRα/β/γ
nuclear receptors to activate mitochondrial gene programmes. Opposite logic — inhibitor
vs agonist.

Full article:

5-Amino-1MQ vs SLU-PP-332: Inhibitor versus Agonist in Metabolic Research

· References 54–63

Attribute 5-Amino-1MQ SLU-PP-332
Chemical class Small-molecule NNMT inhibitor (quinoline derivative) Synthetic pan-ERRα/β/γ nuclear-receptor agonist
Target Nicotinamide N-methyltransferase (NNMT) — enzyme inhibition54,55 Estrogen-related receptors α, β, γ (ERR) — nuclear receptor agonism58,59
Mechanistic logic Inhibiting NNMT preserves NAD+ and methyl-donor availability; modulates adipose differentiation and metabolic gene expression55 ERR agonism activates PGC-1α-related mitochondrial biogenesis and oxidative-metabolism gene programmes — an “exercise mimetic” approach58,59
Primary preclinical model contexts High-fat-diet obese rodents; HeLa anti-proliferation (in vitro)56; cancer-associated fibroblast models57; pancreatic fibrosis (rodent)63 Aerobic exercise capacity in mice58; metabolic syndrome models59; orally active SLU-PP-915 analogue data60
Format (Condor Research) Vial (lyophilised) · 5-Amino-1MQ Capsules Vial (lyophilised) · SLU-PP-332 Capsules
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical only
Rodent metabolic models; in vitro; no human RCTs; not an approved drug		 Preclinical only
Rodent exercise-capacity models; very early tool-compound status; no human data
How to choose NNMT biology; NAD+/methyl-donor axis; adipogenesis; cancer fibroblast metabolism ERR nuclear-receptor biology; mitochondrial biogenesis; exercise-mimetic model design
5-Amino-1MQ inhibits (enzyme blocker, indirectly raises NAD+); SLU-PP-332 agonises (nuclear receptor activator, turns on mitochondrial gene programmes). Opposite logic, overlapping metabolic-research space.

Supp.
Tesofensine vs Enclomiphene

An atypical pair: different target classes, different research questions, included on
the site as “metabolic / hormonal axis” comparators. Tesofensine is a triple monoamine
reuptake inhibitor studied in CNS and energy-balance models; Enclomiphene is the
trans-isomer of clomiphene, a SERM studied in HPG-axis and gonadotropin models.

Full article:

Tesofensine vs Enclomiphene: A Research-Use Comparison

· References 64–71

Attribute Tesofensine Enclomiphene
Chemical class Triple monoamine reuptake inhibitor (5-HT, DA, NE) Selective estrogen receptor modulator (SERM) — trans-isomer of clomiphene
Target SERT, DAT, NET (serotonin, dopamine, norepinephrine transporters)64 Estrogen receptor (ER antagonist) → HPG axis, LH/FSH release68
Primary mechanism studied (preclinical) Appetite suppression via α1-adrenoceptor and D1R pathways in DIO rats65; improved glycaemic control vs sibutramine/rimonabant66; hypothalamic GABAergic neuron silencing67 ER antagonism → increased LH/FSH → endogenous testosterone in hypogonadal models68,69; preserves sperm counts vs topical testosterone (clinical observation)70
Format (Condor Research) Capsules Capsules
Purity / QC ≥99% HPLC; third-party COA (CZ lab) ≥99% HPLC; third-party COA (CZ lab)
Evidence quality Preclinical + Phase II
Reached Phase II obesity trial; not approved; no EMA/FDA marketing authorisation		 Early human data
Small clinical studies in secondary hypogonadism; not approved by EMA; IND-exempt in some jurisdictions — supplied here strictly as RUO reference material
How to choose CNS monoamine reuptake biology; energy-balance and obesity-model research HPG-axis biology; gonadotropin / testosterone-axis research models
Different targets, different axes. Paired on the site as metabolic/hormonal comparators for researchers navigating body-composition adjacent compound selection. Not therapeutic guidance.

How to Use These Tables

Each table row consolidates specification data already published on condorresearch.com/research/.
No new claims are made. The “Evidence quality” row is the most important: every compound
listed here is at the preclinical stage or early human-data stage in the research context
in which it is supplied. No approved-drug status applies to any compound in the RUO
context supplied here.

Click the article link in each pair header to read the full analysis, including mechanism
sections, evidence-quality discussion, and the complete references list with PMIDs and DOIs.
COA documents are accessible from individual product pages at condorresearch.com.

Frequently Asked Questions

What does ‘research use only’ mean for these compounds?

Research Use Only (RUO) means the compounds are supplied exclusively for qualified in vitro, cell-culture, and animal-model laboratory work. They are not approved drugs, cosmetics, supplements, or food additives. No therapeutic, diagnostic, or veterinary use is implied or permitted. See the full Research Use Only Disclaimer.

Are any of these compounds approved for human use?

No compound listed in this document is approved for human administration in the context it is sold here. Some parent molecules have approved pharmaceutical forms in other jurisdictions (e.g., afamelanotide, tesamorelin, semax in Russia), but those approvals are entirely separate from the RUO reference materials supplied by Condor Research.

How is purity verified across all compounds?

All Condor Research compounds are characterised at ≥99% purity by HPLC and/or mass spectrometry. Third-party, independent batch testing is conducted in the Czech Republic. Lot-specific Certificates of Analysis (COA) are linked from each product page. For the testing framework overview, see Quality & Third-Party Testing.

Can I combine compounds from different comparison pairs in a single study design?

Combination questions follow the experimental design — researchers define readouts, controls, and statistical power independently. Condor Research supplies co-formulated blends (BPC-157 + TB-500, CJC-1295 no DAC + Ipamorelin, GLOW, KLOW) for convenience, but any combination study should be designed and powered as its own experiment. No therapeutic rationale is stated or implied.

Where can I find lot-specific COA data?

Each product page on condorresearch.com links to its current COA. The Quality & Third-Party Testing page provides a centralised overview of the testing framework used for all compounds.

How current are these comparison tables?

Data were consolidated from content published on condorresearch.com in 2025–2026 and reflect the peer-reviewed literature cited on each comparison page. Individual pages carry the date of last review. This document was compiled June 2026.

References

  1. Chang CH et al. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol. 2011;110(3):774–780. PMID 21030672
  2. Cerovecki T et al. Pentadecapeptide BPC 157 (PL 14736) improves ligament healing in the rat. J Orthop Res. 2010;28(9):1155–1161. PMID 20225319
  3. Novinscak T et al. Gastric pentadecapeptide BPC 157 as an effective therapy for muscle crush injury in the rat. Surg Today. 2008;38(8):716–725. PMID 18668315
  4. Chang CH et al. Pentadecapeptide BPC 157 enhances the growth hormone receptor expression in tendon fibroblasts. Molecules. 2014;19(11):19066–19077. PMID 25415472
  5. Sikiric P et al. Cytoprotective gastric pentadecapeptide BPC 157 resolves major vessel occlusion disturbances. World J Gastroenterol. 2022;28(1):23–46. PMID 35125818
  6. Sikiric P et al. The Stable Gastric Pentadecapeptide BPC 157 Pleiotropic Beneficial Activity. Pharmaceuticals. 2024;17(4):461. PMID 38675421
  7. Goldstein AL et al. Thymosin beta4: actin-sequestering protein moonlights to repair injured tissues. Trends Mol Med. 2005;11(9):421–429. PMID 16099219
  8. Philp D, Kleinman HK. Animal studies with thymosin beta, a multifunctional tissue repair and regeneration peptide. Ann N Y Acad Sci. 2010;1194:81–86. PMID 20536453
  9. Philp D et al. The actin binding site on thymosin beta4 promotes angiogenesis. FASEB J. 2003;17(14):2103–2105. PMID 14500546

  10. Schlesinger DH et al. Growth-modulating serum tripeptide is glycyl-histidyl-lysine. Experientia. 1977;33(3):324–325. PMID 858356
  11. Pickart L et al. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. Biomed Res Int. 2015;2015:648108. PMID 26236730
  12. Pickart L, Margolina A. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. Int J Mol Sci. 2018;19(7):1987. PMID 29986520
  13. Trapaidze A et al. Thermodynamic study of Cu2+ binding to the DAHK and GHK peptides by isothermal titration calorimetry. J Biol Inorg Chem. 2012;17(1):37–47. PMID 21898044
  14. Pyo HK et al. The effect of tripeptide-copper complex on human hair growth in vitro. Arch Pharm Res. 2007;30(7):834–839. PMID 17703734
  15. Jung JI et al. Vitamin C-linker-conjugated tripeptide AHK stimulates BMP-2-induced osteogenic differentiation. Differentiation. 2018;101:1–7. PMID 29567599
  16. Gonzalez P et al. Why the Ala-His-His Peptide Is an Appropriate Scaffold to Remove and Redox Silence Copper Ions. Biomolecules. 2022;12(10):1327. [Related scaffold; family context for AHK-Cu.] PMID 36291536
  17. Mehr A et al. The copper(II)-binding tripeptide GHK, a valuable crystallization and phasing tag. Acta Crystallogr D. 2020;76(Pt 12):1222–1232. PMID 33263328

  18. Raun K et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552–561. PMID 9849822
  19. Johansen PB et al. Pharmacokinetic evaluation of ipamorelin and other peptidyl growth hormone secretagogues. Xenobiotica. 1998;28(11):1083–1092. PMID 9879640
  20. Venkova K et al. Efficacy of ipamorelin, a novel ghrelin mimetic, in a rodent model of postoperative ileus. J Pharmacol Exp Ther. 2009;329(3):1110–1116. PMID 19289567
  21. Jetté L et al. Human GRF1-29-albumin bioconjugates activate the GRF receptor; identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052–3058. PMID 15817669
  22. Teichman SL et al. Prolonged stimulation of GH and IGF-I secretion by CJC-1295 in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799–805. PMID 16352683
  23. Ionescu M, Frohman LA. Pulsatile secretion of GH persists during continuous stimulation by CJC-1295. J Clin Endocrinol Metab. 2006;91(12):4792–4797. PMID 17018654
  24. Sackmann-Sala L et al. Activation of the GH/IGF-1 axis by CJC-1295 results in serum protein profile changes. Growth Horm IGF Res. 2009;19(6):471–477. PMID 19386527
  25. Alba M et al. Once-daily administration of CJC-1295 normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290–E1294. PMID 16822960

  26. Vyunova TV et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein Pept Lett. 2018;25(10):914–923. PMID 30255741
  27. Filatova E et al. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. Front Pharmacol. 2017;8:89. PMID 28293190
  28. Kolik LG et al. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating BDNF Content. Bull Exp Biol Med. 2019;167(5):641–644. PMID 31625062
  29. Kasian A et al. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats. Behav Neurol. 2017;2017:5091027. PMID 28280289
  30. Zozulya AA et al. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders. Zh Nevrol Psikhiatr. 2008;108(4):38–48. PMID 18454096
  31. Sciacca MFM et al. Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Aβ Aggregation and Amyloid Formation. ACS Chem Neurosci. 2022;13(4):486–496. PMID 35080861
  32. Stavchansky VV et al. Insight into Glyproline Peptides’ Activity through the Modulation of Inflammatory and Neurosignaling Genetic Response Following Cerebral Ischemia-Reperfusion. Genes (Basel). 2022;13(12):2380. PMID 36553646
  33. Inozemtseva LS et al. Antidepressant-like and antistress effects of the ACTH(4-10) synthetic analogs Semax and Melanotan II on male rats. Eur J Pharmacol. 2024;984:177068. PMID 39442746
  34. Panikratova YR et al. Functional Connectomic Approach to Studying Selank and Semax Effects. Dokl Biol Sci. 2020;490(1):9–11. PMID 32342318
  35. Gusev EI et al. The efficacy of semax in the treatment of patients at different stages of ischemic stroke. Zh Nevrol Psikhiatr. 2018;118(3 Pt 2):61–68. PMID 29798983

  36. Covarrubias AJ et al. NAD+ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol. 2021;22(2):119–141. PMID 33353981
  37. Verdin E. NAD+ in aging, metabolism, and neurodegeneration. Science. 2015;350(6265):1208–1213. PMID 26785480
  38. Mills KF et al. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016;24(6):795–806. PMID 28068222
  39. Rajman L et al. Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metab. 2018;27(3):529–547. PMID 29514064
  40. Grozio A et al. Slc12a8 is a nicotinamide mononucleotide transporter. Nat Metab. 2019;1(1):47–57. PMID 31131364
  41. Yoshino M et al. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science. 2021;372(6547):1224–1229. PMID 33888596
  42. Irie J et al. Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels. Endocr J. 2020;67(2):153–160. PMID 31685720
  43. Wen J et al. Improved Physical Performance Parameters in Patients Taking NMN: A Systematic Review of Randomized Control Trials. Cureus. 2024;16(8):e65961. PMID 39221308
  44. Vinten KT et al. NAD+ precursor supplementation in human ageing: clinical evidence and challenges. Nat Metab. 2025;7(10):1974–1990. PMID 41083806

  45. Khavinson VKh et al. Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bull Exp Biol Med. 2003;135(6):590–592. PMID 12937682
  46. Khavinson VKh. Peptides and Ageing. Neuro Endocrinol Lett. 2002;23 Suppl 3:11–144. PMID 12374906
  47. Anisimov VN et al. Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice. Biogerontology. 2003;4(4):193–202. PMID 14501183
  48. Khavinson VKh, Morozov VG. Peptides of pineal gland and thymus prolong human life. Neuro Endocrinol Lett. 2003;24(3-4):233–240. PMID 14523363
  49. Khavinson V et al. Pinealon increases cell viability by suppression of free radical levels and activating proliferative processes. Rejuvenation Res. 2011;14(5):535–541. PMID 21978084
  50. Khavinson V et al. EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer’s Disease. Molecules. 2020;26(1):159. PMID 33396470
  51. Khavinson V et al. Neuroprotective Effects of Tripeptides-Epigenetic Regulators in Mouse Model of Alzheimer’s Disease. Pharmaceuticals (Basel). 2021;14(6):515. PMID 34071923
  52. Arutjunyan A et al. Pinealon protects the rat offspring from prenatal hyperhomocysteinemia. Int J Clin Exp Med. 2012;5(2):179–185. PMID 22567179

  53. Neelakantan H et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141–152. PMID 29155147
  54. Kraus D et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508(7495):258–262. PMID 24717514
  55. Akar S et al. Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells. J Obstet Gynaecol. 2021;41(8):1240–1245. PMID 33645410
  56. Yang M et al. NAD+ metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression. J Immunother Cancer. 2024;12(7):e009281. PMID 39067875
  57. Ren N et al. NNMT Inhibition Mitigates Cerulein-Induced Pancreatic Fibrosis. Inflammation. 2026;49(1):135. PMID 41904718
  58. Billon C et al. Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response. ACS Chem Biol. 2023;18(4):756–771. PMID 36988910
  59. Billon C et al. A Synthetic ERR Agonist Alleviates Metabolic Syndrome. J Pharmacol Exp Ther. 2024;388(2):232–240. PMID 37739806
  60. Billon C et al. An orally active estrogen receptor-related receptor agonist, SLU-PP-915, enhances aerobic exercise capacity. J Pharmacol Exp Ther. 2026;393(1):103787. PMID 41421047
  61. de Souza-Lima J et al. Pharmacological Activation of ERRα/β/γ as an Exercise Mimetic. Rev Med Chil. 2026;154(2):237–245. PMID 42024694
  62. Prajapati S et al. Nicotinamide N-Methyltransferase (NNMT): A Central Regulator in Hepatocellular Carcinoma Metabolism — A Systematic Review. Curr Drug Metab. 2026 Jun 4. PMID 42260786

  63. Bello NT, Zahner MR. Tesofensine, a monoamine reuptake inhibitor for the treatment of obesity. Curr Opin Investig Drugs. 2009;10(10):1105–1116. PMID 19777399
  64. Axel AM et al. Tesofensine, a novel triple monoamine reuptake inhibitor, induces appetite suppression by indirect stimulation of alpha1 adrenoceptor and dopamine D1 receptor pathways. Neuropsychopharmacology. 2010;35(7):1464–1476. PMID 20200509
  65. Hansen HH et al. The novel triple monoamine reuptake inhibitor tesofensine induces sustained weight loss and improves glycaemic control. Eur J Pharmacol. 2010;636(1-3):88–95. PMID 20385125
  66. Perez CI et al. Tesofensine, a novel antiobesity drug, silences GABAergic hypothalamic neurons. PLoS One. 2024;19(4):e0300544. PMID 38656972
  67. Hill S et al. Enclomiphene, an estrogen receptor antagonist for the treatment of testosterone deficiency in men. IDrugs. 2009;12(2):109–119. PMID 19204885
  68. Rodriguez KM et al. Enclomiphene citrate for the treatment of secondary male hypogonadism. Expert Opin Pharmacother. 2016;17(11):1561–1567. PMID 27337642
  69. Kim ED et al. Oral enclomiphene citrate raises testosterone and preserves sperm counts in obese hypogonadal men. BJU Int. 2016;117(4):677–685. PMID 26496621
  70. Tienforti D et al. Selective modulation of estrogen receptor in obese men with androgen deficiency: A systematic review and meta-analysis. Andrology. 2023. PMID 36604313

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