Forward thinking to
reverse cell ageing

Developing a new generation of senotherapeutic interventions to target the diseases and aesthetic signs of ageing.

Photo of Astrocyte cells. Senescent primary astrocyte cells.
Image credit: Dr Eva Latorre, Harries Lab.

About Us

SENISCA is a biotech spinout company from the University of Exeter, founded in 2020 and dedicated to the development of new approaches to reverse cellular senescence (senotherapeutics).

Our founders are world leaders in molecular and cellular biology and have patent-protected an innovation for the reversal of cellular senescence. This innovation works by restoring the ability of cells to ‘fine tune’ the expression of their genes to rejuvenate aged cells.

At SENISCA, we are using this knowledge, concerning how and why cells become senescent, to develop a new generation of oligonucleotide-based interventions, to turn back the ageing clock in old cells and to target the diseases and aesthetic signs of ageing.

Photo of fibroblast cells 48 hour timelapse of rejuvenating senescent primary human dermal fibroblast cells.
Image credit: Dr Eva Latorre, Harries Lab.

Scientific Approach

A major cause of age-related diseases and the aesthetic signs of ageing is the accumulation of senescent cells in aged tissues and organs; removal of such cells has been shown to be capable of bringing about ‘rejuvenation’ of function in people and animals. At SENISCA, we have discovered a new and druggable means to reverse senescence through modulation of RNA splicing.

When genes are switched on, they make a message (mRNA), containing the instructions to make whatever the cell requires. Most genes can make more than one type of mRNA message (mRNA isoform), depending on the needs of the cell in a process termed ‘alternative splicing’. The balance of mRNA isoforms made from each gene is critical and underpins the ability of cells to adapt and respond to their environment. This ability to ‘fine tune’ gene outputs is vital for long-term health. The choice of which isoforms are produced is made by a set of regulatory proteins (collectively termed splicing factors).

Our founders have discovered that levels of splicing factors change during ageing, compromising our ability to carry out this ‘fine tuning’ of gene expression. This is a fundamental reason why cells become senescent. Compromised molecular resilience is a major cause of the ill health and frailty that accompanies ageing. We have demonstrated that restoration of splicing factor levels to those seen in younger cells is able to effectively turn back the ageing clock in old cells, bringing about reversal of senescence.

At SENISCA, we are using oligonucleotide-based therapeutic approaches to reset splicing factor levels and reverse senescence. We anticipate that understanding the molecular basis of rejuvenation will highlight new treatments for the diseases and aesthetic aspects of ageing. More importantly, it is likely that preventative approaches based on rejuvenation will be developed reducing both disease incidence and severity.

Photo of Fibroblast cells background First overlay image of Fibroblast cells Second overlay image of Fibroblast cells Proliferating primary human fibroblast cells.
Image credit: Dr Nicola Jeffery, Harries Lab.

The Team


Research Team

Board Advisory

News & Events

Press Release

Nature Spinoff prize

SENISCA shortlisted for 2022/2023 Nature Spinoff prize.

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Press Release

Senisca new appointments

Senisca announce the expansion of its leadership team with the appointment of Dr. Sarah Cole as Chief Operating Officer, Dr. Tim Schmidt as Chief Development Officer and Dr. Adam Clauss as VP Dermatology.

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Press Release

Senisca Innovate UK Grant

SENISCA awarded Innovate UK grant to develop oligonucleotide therapeutics for the treatment of idiopathic pulmonary fibrosis (IPF).

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Media Articles

Nature Biotechnology. November 2020

Send in the senolytics.

News Feature Find Out More

INTERVIEW: Longevity Technology. July 2020.

SENISCA seeks funding for senescence reversal.

Professor Lorna Harries Find Out More

INVITED REVIEW Frontiers in Genetics 2019.

RNA Biology Provides New Therapeutic Targets for Human Disease.

Professor Lorna Harries Find Out More

Nature Outlook. October 2019.

It’s time for scientists to shout about RNA therapies.

Professor Lorna Harries Find Out More


SENISCA will be attending the following conferences:

  • BioTrinity: 25th - 26th April 2023 (London)
  • BioEquity: 14th - 16th May 2023 (Dublin)
  • Next Gen Inhalation Delivery summit 2023: 20th - 22nd June 2023 (Boston)

Lorna Harries (CSO) will be speaking at:

  • 5th Age Related Disease Therapeutics Summit 2023: 31st May - 2nd June 2023 (San Francisco)
  • Proteomass splicing meeting 2023: 17th - 21st July 2023 (Lisbon)
Photo of Fibroblast cells Senescent primary human fibroblast cells.
Image credit: Emad Manni, Harries Lab.


We are looking for talented, innovative, passionate and visionary staff to join our growing team and help us realise the incredible potential of SENISCA's senotherapeutic technology. Please send CV's and initial enquiries to addressed to Jennie Jepperson (SENISCA's Executive Assistant) We look forward greatly to hearing from you.


  1. Manni E, Jeffery N, Chambers D, Slade L, Etheridge T, Harries LW. "An evaluation of the role of miR-361-5p in senescence and systemic ageing." Exp Gerontol. 2023 Apr;174:112127. Epub 2023 Feb 18. doi: 10.1016/j.exger.2023.112127
  2. Harries LW. FEBS J. "Dysregulated RNA processing and metabolism: a new hallmark of ageing and provocation for cellular senescence". 2023 Mar;290(5):1221-1234. Epub 2022 Apr 29.doi: 10.1111/febs.16462
  3. Frankum R, Jameson TSO, Knight BA, Stephens FB, Wall BT, Donlon TA, Torigoe T, Willcox BJ, Willcox DC, Allsopp RC, Harries LW. "Extreme longevity variants at the FOXO3 locus may moderate FOXO3 isoform levels". Geroscience. 2022 Apr;44(2):1129-1140. Epub 2021 Aug 26. doi: 10.1007/s11357-021-00431-0
  4. Lee BP, Harries LW. "Senotherapeutic Drugs: A New Avenue for Skincare?". Plast Reconstr Surg. 2021 Dec 1;148(6S):21S-26S. doi: 10.1097/PRS.0000000000008782
  5. Bramwell LR, Harries LW. "Targeting Alternative Splicing for Reversal of Cellular Senescence in the Context of Aesthetic Aging". Plast Reconstr Surg. 2021 Jan 1;147(1S-2):25S-32S. doi: 10.1097/PRS.0000000000007618
  6. Frankum R, Jameson TSO, Knight BA, Stephens FB, Wall BT, Donlon TA, Torigoe T, Willcox BJ, Willcox DC, Allsopp RC, Harries LW. "Extreme longevity variants at the FOXO3 locus may moderate FOXO3 isoform levels." Geroscience. (2021). doi: 10.1007/s11357-021-00431-0. Online ahead of print.PMID: 34436732
  7. Bramwell LR, Harries LW. Targeting Alternative Splicing for Reversal of Cellular Senescence in the Context of Aesthetic Aging. Plast Reconstr Surg. 147(1S-2):25S-32S. (2021) doi: 10.1097/PRS.0000000000007618.PMID: 33347071
  8. Lee BP, Smith M, Buffenstein R & Harries LW. “Negligible senescence in naked mole rats may be a consequence of well-maintained splicing regulation.” GeroScience. 42(2), 633-651 (2020). doi:10.1007/s11357-019-00150-7
  9. Lye JJ*, Latorre E*, Lee BP, Bandinelli S, Holley JE, Gutowski NJ, Ferrucci L & Harries LW. “Astrocyte senescence may drive alterations in GFAPA, CDKN2A p14ARF and TAU3 transcript expression and contribute to cognitive decline.” GeroScience. 41(5), 561-573 (2019). doi: 10.1007/s11357-019-00100-3
  10. Latorre E, Ostler EL, Faragher RGA & Harries LW. “FOXO1 and ETV6 genes may represent novel regulators of splicing factor expression in cellular senescence.” FASEB J. 33(1), 1086-1097 (2019). doi: 10.1096/fj.201801154R
  11. Lee BP, Mulvey L, Barr G, Garratt J, Goodman E, Selman C & Harries LW. “Dietary restriction in ILSXISS mice is associated with widespread changes in splicing regulatory factor expression levels.” Exp Gerontol. 128, 110736 (2019). doi: 10.1016/j.exger.2019.110736
  12. Lee BP, Pilling LC, Bandinelli S, Ferrucci L, Melzer D & Harries LW. “The transcript expression levels of HNRNPM, HNRNPA0 and AKAP17A splicing factors may be predictively associated with ageing phenotypes in human peripheral blood.” Biogerontology. 20(5), 649-663 (2019). doi: 10.1007/s10522-019-09819-0
  13. Latorre E, Birar VC, Sheerin AN, Jeynes JCC, Hooper A, Dawe HR, Melzer D, Cox LS, Faragher RGA, Ostler EL & Harries LW. “Small molecule modulation of splicing factor expression is associated with rescue from cellular senescence.” BMC Cell Biol. 18(1), 31 (2017). doi: 10.1186/s12860-017-0147-7
  14. Latorre E, Torregrossa R, Wood ME, Whiteman M & Harries LW. “Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2.” Aging (Albany NY). 10(7), 1666-1681 (2018). doi: 10.18632/aging.101500
  15. Latorre E, Pilling LC, Lee BP, Bandinelli S, Melzer D, Ferrucci L & Harries LW. “The VEGFA156b isoform is dysregulated in senescent endothelial cells and may be associated with prevalent and incident coronary heart disease.” Clin Sci (Lond). 132(3), 313-325 (2018). doi: 10.1042/CS20171556
  16. Lee BP, Pilling LC, Emond F, Flurkey K, Harrison DE, Yuan R, Peters LL, Kuchel GA, Ferrucci L, Melzer D & Harries LW. “Changes in the expression of splicing factor transcripts and variations in alternative splicing are associated with lifespan in mice and humans.” Aging Cell. 15(5), 903-13 (2016). doi: 10.1111/acel.12499
  17. Holly AC, Melzer D, Pilling LC, Fellows AC, Tanaka T, Ferrucci L & Harries LW. “Changes in splicing factor expression are associated with advancing age in man.” Mech Ageing Dev. 134(9), 356-66 (2013). doi: 10.1016/j.mad.2013.05.006
  18. Harries LW, Hernandez D, Henley W, Wood A, Holly AC, Bradley-Smith RM, Yaghootkar H, Dutta A, Murray A, Frayling TM, Guralnik JM, Bandinelli S, Singleton A, Ferrucci L & Melzer D. “Human aging is characterized by focused changes in gene expression and deregulation of alternative splicing.” Aging Cell. 10(5), 868-78 (2011). doi: 10.1111/j.1474-9726.2011.00726.x


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Photo of Endothelial cells Senescent primary human endothelial cells.
Image credit: Emad Manni, Harries Lab.