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Illustration of cells under a microscope for longevity research

Research area

Senolytics & Longevity Research

Cellular senescence, mitochondrial function and NAD+ metabolism are among the most active areas of ageing biology. This section brings together plain-English summaries of the published literature, a glossary of key terms, and the research compounds we supply for laboratory work in this field, with links to their Certificates of Analysis.

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Why this research area matters to laboratories

Over the past decade, researchers have described a set of recurring biological changes associated with ageing, sometimes called the “hallmarks of ageing”. They include the accumulation of senescent cells, mitochondrial dysfunction, altered nutrient sensing and telomere attrition [1]. Senescent cells have been characterised in cell culture and in animal tissues, and the field has worked to agree common definitions and markers [2].

These topics are studied with a wide range of tools: cell culture models, rodent models, biochemical assays and analytical chemistry. The pages in this section summarise what has been reported in the peer-reviewed literature, state the model used in each study, and link to the original sources so readers can assess the evidence for themselves.

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Research compounds in this area

Each compound is supplied for in-vitro laboratory research only. Select a product to view its specifications. Certificates of Analysis are published on our Verification page.

NAD+ and copper peptides

NAD+

Price: 100mg £14.99 · 500mg £44.99 · 1000mg £74.99

Certificate of Analysis: NAD+ 1000mg, report LDA22161142 (Lingda Laboratory, tested 3 September 2026, HPLC purity >99.77%). View certificates on our Verification page

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GHK-Cu

Price: 50mg £21.99 · 100mg £32.99

Certificates of Analysis: 50mg, report LDA22160942 (tested 1 September 2026, HPLC purity >99.68%); 100mg, report LDA22160952 (tested 2 September 2026, >99.75%). Lingda Laboratory. View certificates on our Verification page

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Klow-80

Price: 80mg £69.99

Certificate of Analysis: report LDA22161252 (Lingda Laboratory, tested 3 September 2026, HPLC purity >99.72%). View certificates on our Verification page

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Made to order

Epitalon

Price: 10mg £18.99 · 50mg £44.99

Made to order: please allow 14–16 days in total, including delivery.

Certificates of Analysis: 10mg (report LDA22161072) and 50mg (report LDA22161082). View certificates on our Verification page

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MOTS-c

Price: 10mg £27.99 · 20mg £42.99 · 40mg £69.99

Made to order: please allow 14–16 days in total, including delivery.

Certificates of Analysis: 10mg (Bio-Analysis Centre), 20mg (report LDA22160992) and 40mg (report LDA22161002). View certificates on our Verification page

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SS-31

Price: 10mg £34.99 · 50mg £134.99

Made to order: please allow 14–16 days in total, including delivery.

Certificate of Analysis: 50mg (report LDA22161222). View certificates on our Verification page

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FOXO4-DRI

Price: 10mg £149.99

Made to order: please allow 14–16 days in total, including delivery.

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Latest research updates

Research update: long-term senolytic treatment and exercise in the ageing mouse heart

Testing and transparency

Our research compounds are tested by third-party laboratories. Certificates of Analysis are published on our Verification page and show the testing laboratory, report number, test date and the analytical results (for example HPLC purity).

Common questions

Do you sell senolytic drugs such as dasatinib, quercetin or fisetin?

No. These compounds are discussed in our articles as background to the published literature only. They are not sold by Corex Vitality™.

Are these products for human use?

No. All Corex Vitality™ products are supplied strictly for laboratory research use only. They are not for human or veterinary use, and we do not provide administration, protocol or usage guidance.

Why do some products have a longer delivery time?

Epitalon, MOTS-c, SS-31 and FOXO4-DRI are made to order. Please allow 14–16 days in total, including delivery.

Where do your references come from?

Every science article cites peer-reviewed publications with links to PubMed or the publisher (DOI), so you can read the original study.

See all longevity research FAQs

Longevity Research Digest

Monthly summaries of new published research, new certificates and new stock. Sign-up opens soon.

Research use only. Corex Vitality™ products are supplied for laboratory research purposes only and are not intended for human or veterinary use, or for the diagnosis, treatment, prevention or cure of any disease or medical condition. Content in this section summarises published scientific literature for educational purposes. It does not describe the effects of any Corex Vitality™ product and should not be read as a claim about any product.

References

  1. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: an expanding universe. Cell. 2023;186(2):243-278. PubMed: https://pubmed.ncbi.nlm.nih.gov/36599349/ · DOI: https://doi.org/10.1016/j.cell.2022.11.001
  2. Gorgoulis V, et al. Cellular senescence: defining a path forward. Cell. 2019;179(4):813-827. PubMed: https://pubmed.ncbi.nlm.nih.gov/31675495/ · DOI: https://doi.org/10.1016/j.cell.2019.10.005

Research you can verify.

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📚 Peer-Reviewed Literature · PubMed Indexed

Published Research — Peer-Reviewed Receptor & Pathway Studies

NCBI PubMed Database ↗ Verify Batch COAs →

NAD+ (Nicotinamide Adenine Dinucleotide)

  1. [1] Ramsey KM et al. · Science (2009)

    Molecular and murine biochemical study demonstrating that nicotinamide phosphoribosyltransferase (NAMPT) and intracellular NAD+ levels oscillate under CLOCK:BMAL1 transcriptional control to regulate SIRT1 deacetylase activity.

    PMID: 19299583 ↗ DOI: 10.1126/science.1171641 ↗
  2. [2] Gomes AP et al. · Cell (2013)

    Cellular and murine bioenergetics study showing that nuclear NAD+ depletion reduces SIRT1 activity and stabilises HIF-1α under normoxic conditions, downregulating mitochondrially encoded oxidative phosphorylation (OXPHOS) subunits.

    PMID: 24360282 ↗ DOI: 10.1016/j.cell.2013.11.037 ↗
  3. [3] Cantó C et al. · Cell Metab (2015)

    Mechanistic review of subcellular NAD+ compartmentalisation, salvage-pathway enzymatic synthesis, sirtuin and PARP cosubstrate consumption, and the mitochondrial unfolded protein response (UPRmt).

    PMID: 26118927 ↗ DOI: 10.1016/j.cmet.2015.05.023 ↗
  4. [4] Camacho-Pereira J et al. · Cell Metab (2016)

    Enzymatic and knockout-mouse study identifying the ectoenzyme NADase CD38 as a primary regulator of cellular NAD+ degradation, mitochondrial oxygen consumption, and SIRT3-dependent protein deacetylation.

    PMID: 27304511 ↗ DOI: 10.1016/j.cmet.2016.05.006 ↗

Epitalon (AEDG Pineal Tetrapeptide)

  1. [1] Khavinson VKh et al. · Bull Exp Biol Med (2003)

    In-vitro telomerase-negative human fetal lung fibroblast (KMST-6) culture study demonstrating induction of hTERT catalytic subunit expression, telomerase enzymatic activity, and telomere length elongation.

    PMID: 12937682 ↗ DOI: 10.1023/a:1025493705728 ↗
  2. [2] Khavinson V et al. · Molecules (2020)

    Immunofluorescence, RT-qPCR, and molecular docking investigation showing that the Ala-Glu-Asp-Gly (AEDG) tetrapeptide binds histone H1/3/6/H4 complexes and upregulates Nestin, GAP43, β-tubulin III, and Doublecortin expression in cultured stem cells.

    PMID: 32019204 ↗ DOI: 10.3390/molecules25030609 ↗
  3. [3] Araj SK et al. · Int J Mol Sci (2025)

    Comprehensive biochemical review of the synthetic tetrapeptide Ala-Glu-Asp-Gly (Epitalon), detailing its telomerase activation pathways, reactive oxygen species scavenging, and epigenetic chromatin interactions in cellular models.

    PMID: 40141333 ↗ DOI: 10.3390/ijms26062691 ↗
  4. [4] Al-Dulaimi S et al. · Biogerontology (2025)

    Comparative in-vitro study across normal epithelial and immortalised cell lines quantifying hTERT mRNA expression, telomerase enzyme activity, and alternative lengthening of telomeres (ALT) promyelocytic leukaemia bodies.

    PMID: 40908429 ↗ DOI: 10.1007/s10522-025-10315-x ↗

SS-31 (Elamipretide / D-Arg-Dmt-Lys-Phe-NH2)

  1. [1] Birk AV et al. · J Am Soc Nephrol (2013)

    Fluorescence spectroscopy and Oxygraph respirometry study demonstrating that the aromatic-cationic tetrapeptide SS-31 binds selectively to inner-mitochondrial-membrane cardiolipin with 1:1 stoichiometry, preventing cytochrome c peroxidase conversion and preserving ATP synthesis.

    PMID: 23813215 ↗ DOI: 10.1681/ASN.2012121216 ↗
  2. [2] Mitchell W et al. · J Biol Chem (2020)

    Biophysical and 31P/2H solid-state NMR study showing that SS-31 partitions into cardiolipin-rich anionic lipid bilayers to down-regulate membrane surface electrostatic potential and prevent divalent calcium-induced lipid packing stress.

    PMID: 32273339 ↗ DOI: 10.1074/jbc.RA119.012094 ↗
  3. [3] Mitchell W et al. · Elife (2022)

    High-resolution structural and biophysical analysis of sixteen SS-31 tetrapeptide variants evaluating aromatic side-chain composition, bilayer insertion depth, membrane surface charge modulation, and cellular ATP production.

    PMID: 35913044 ↗ DOI: 10.7554/eLife.75531 ↗
  4. [4] Campbell MD et al. · Geroscience (2022)

    Quantitative mass-spectrometry phosphoproteomics and mitochondrial respiration study in murine skeletal muscle mapping post-translational phosphorylation changes across electron-transport-chain and metabolic signalling proteins.

    PMID: 36322234 ↗ DOI: 10.1007/s11357-022-00679-0 ↗

MOTS-c (Mitochondrial-Derived Peptide)

  1. [1] Lee C et al. · Cell Metab (2015)

    Discovery study identifying a 16-amino-acid peptide encoded within a short open reading frame (sORF) of mitochondrial 12S rRNA that inhibits the folate-methionine cycle, accumulates endogenous AICAR, and activates AMPK in cultured cells.

    PMID: 25738459 ↗ DOI: 10.1016/j.cmet.2015.02.009 ↗
  2. [2] Kim KH et al. · Cell Metab (2018)

    Cell-biology and chromatin-binding study demonstrating AMPK-dependent nuclear translocation of MOTS-c under glucose restriction and direct interaction with ARE-regulated stress transcription factors including NRF2 (NFE2L2).

    PMID: 29983246 ↗ DOI: 10.1016/j.cmet.2018.06.008 ↗
  3. [3] García-Benlloch S et al. · Peptides (2022)

    In-vitro human (LHCN-M2) and murine (C2C12) myoblast culture study showing that wild-type MOTS-c, via its conserved YIFY Src-homology-2 (SH2)-like motif, inhibits IL-6-induced STAT3 transcriptional activity and promotes myotube formation.

    PMID: 35842023 ↗ DOI: 10.1016/j.peptides.2022.170840 ↗
  4. [4] Kumagai H et al. · iScience (2024)

    Cell-free biophysical and murine signalling study identifying casein kinase 2 (CK2) as a direct binding partner of MOTS-c and comparing wild-type vs K14Q variant peptide-protein interaction kinetics.

    PMID: 39559755 ↗ DOI: 10.1016/j.isci.2024.111212 ↗

FOXO4-DRI (D-Retro-Inverso FOXO4 Peptide)

  1. [1] Baar MP et al. · Cell (2017)

    Foundational study designing the cell-permeable D-retro-inverso peptide FOXO4-DRI, demonstrating competitive disruption of nuclear FOXO4–p53 PML-body complexes, p53 nuclear exclusion, and selective caspase-3/7-mediated apoptosis in senescent cells.

    PMID: 28340339 ↗ DOI: 10.1016/j.cell.2017.02.031 ↗
  2. [2] Huang Y et al. · Front Bioeng Biotechnol (2021)

    In-vitro serial population-doubling culture study demonstrating that FOXO4-DRI selectively clears SA-β-gal-positive senescent chondrocytes and reduces senescence-associated secretory phenotype (SASP) marker expression.

    PMID: 33996787 ↗ DOI: 10.3389/fbioe.2021.677576 ↗
  3. [3] Kim J et al. · FEBS J (2022)

    NMR spectroscopy and isothermal titration calorimetry (ITC) study mapping the molecular binding interface between the FOXO4 forkhead-associated domain and the p53 transactivation domain.

    PMID: 34954873 ↗ DOI: 10.1111/febs.16333 ↗
  4. [4] Bourgeois B et al. · Nat Commun (2025)

    High-resolution NMR, small-angle X-ray scattering (SAXS), and biochemical study demonstrating that FOXO4-DRI directly binds the intrinsically disordered p53 transactivation domain (TAD) with higher affinity than native FOXO4.

    PMID: 40593617 ↗ DOI: 10.1038/s41467-025-60844-9 ↗

GHK-Cu (Copper Tripeptide-1)

  1. [1] Pickart L et al. · Nature (1980)

    Foundational biochemical and structure-function study demonstrating that the histidyl-lysyl tripeptide chelates copper(II) in equimolar coordination and facilitates cellular copper transport in cultured hepatoma cells.

    PMID: 7453802 ↗ DOI: 10.1038/288715a0 ↗
  2. [2] Maquart FX et al. · FEBS Lett (1988)

    In-vitro fibroblast culture study showing picomolar-to-nanomolar (10^-12 to 10^-9 M) stimulation of collagen biosynthesis by the GHK–Cu(II) coordination complex independent of cell-number changes.

    PMID: 3169264 ↗ DOI: 10.1016/0014-5793(88)80509-x ↗
  3. [3] Wegrowski Y et al. · Life Sci (1992)

    Radiolabelled [3H]-glucosamine and [35S]-sulfate incorporation assay in cultured human fibroblasts demonstrating biphasic stimulation of extracellular dermatan sulfate and cell-layer heparan sulfate synthesis at 10^-9 to 10^-8 M GHK-Cu.

    PMID: 1522753 ↗ DOI: 10.1016/0024-3205(92)90504-i ↗
  4. [4] Mehr A et al. · Acta Crystallogr D Struct Biol (2020)

    X-ray crystallographic structural study resolving the high-affinity square-pyramidal copper(II) coordination sphere formed by the N-terminal GHK tripeptide motif in recombinant fusion proteins.

    PMID: 33263328 ↗ DOI: 10.1107/S2059798320013741 ↗

KLOW-80 Quad-Blend (GHK-Cu + BPC-157 + TB-500 + KPV)

  1. [1] Chavatte P et al. · J Pharm Pharmacol (2001)

    Two-dimensional 1H-NMR spectroscopy and molecular-mechanics conformational analysis of the α-MSH(11–13) C-terminal tripeptide Ac-Lys-Pro-Val-NH2 (KPV), defining its folded trans-proline secondary structure in solution.

    PMID: 11480545 ↗ DOI: 10.1211/0022357011776360 ↗
  2. [2] Dalmasso G et al. · Gastroenterology (2008)

    In-vitro Caco-2, HT29-Cl.19A, and Jurkat T-cell study demonstrating that the oligopeptide transporter PepT1 mediates intracellular uptake of the KPV tripeptide to inhibit NF-κB and MAPK pro-inflammatory signalling cascades.

    PMID: 18061177 ↗ DOI: 10.1053/j.gastro.2007.10.026 ↗
  3. [3] Land SC · Int J Physiol Pathophysiol Pharmacol (2012)

    In-vitro bronchial epithelial cell study demonstrating that the tripeptide KPV suppresses TNF-α- and respiratory syncytial virus-induced NF-κB nuclear translocation and IL-8/eotaxin chemokine secretion.

    PMID: 22837805 ↗
  4. [4] Songok AC et al. · PLoS One (2018)

    Synthetic peptide chemistry and NMR spectroscopic characterisation of modified Lys-Pro-Val (KPV) tripeptide derivatives engineered to resist proteolytic aminopeptidase degradation in biological matrices.

    PMID: 29953505 ↗ DOI: 10.1371/journal.pone.0199686 ↗

References are provided for scientific context only. All Corex Vitality™ compounds are supplied strictly for in-vitro laboratory research use (RUO).