What is RES™?

Regenerative Epithelial Suspension™ – RES™ – is an autologous suspension composed of the cells and wound-healing factors necessary to regenerate natural healthy skin.

Avita’s unique regenerative technology enables clinicians to rapidly create and apply RES™ at the point of care in a simple 30-minute procedure.

The regenerative mechanism is within the suspension…

Activated – Disaggregation of skin cells removes contact inhibition, inducing the “free edge” effect2  which initiates a cascade of wound healing cell signals.14

Growth factors and cytokines are rapidly secreted by “free edge” keratinocytes and fibroblasts to orchestrate proliferation, migration, angiogenesis and matrix re-modelling processes which are essential for skin regeneration.3-13

In laboratory experiments, RES™ has been shown to exhibit the characteristics of cells in the “free edge” state. Investigators found that large numbers of viable cells from RES™ adhere to a wound bed almost instantly and displayed typical proliferative and migratory morphologies as early as day 1 post-harvest. Key proteins (Involucrin and P-ERK) associated with activation were shown to increase and decrease, in accordance with the literature.14

Available – RES™ is available within minutes at the point of care and delivers non-cultured disaggregated skin cells which trigger signalling across the surface of the wound, overcoming the usual limitations of the wound edge.1,15-19

Autologous – The patient is the donor: RES™ is produced from the patient’s skin. In addition, there is no risk of an adverse immune response.20

Complete – The multi-phenotype skin cells1 contained in RES™ are essential in the normal cellular processes for effective wound healing and restoration of normal functionality (e.g. durability, pigmentation, minimal contracture).21

Melanocytes contained in RES™ survive to localize to the epidermal side of the dermal-epidermal junction and evenly distribute melanin throughout the epidermis for pigmentation of the new skin.22

Application of RES™ increases the number of resident fibroblasts in the wound to reduce migration and wound tension,23-25 which reduces the incidence of contracture.

Simple. Safe. Effective.

  • A single use medical device

  • Used at the point of care

  • Prepares RES™ in as little as 30 minutes


  1. Wood FM, Giles N, Stevenson A, Rea S, Fear M. Characterisation of the cell suspension harvested from the dermal epidermal junction using a ReCell® kit. Burns 2012; 38:44-51.
  2. Singer AJ, Clark RAF. Cutaneuous wound healing. New England Journal of Medicine 1999; 341(10):739-746.
  3. Mizutani H, Black R, Kupper TS. Human keratinocytes produce but do not process pro-interleukin-1 (IL-1) beta, different strategies of IL-1 production and processing in monocytes and keratinocytes. Journal of Clinical Investigation 1991; 87:1066-1071.
  4. Wood LC, Elias PM, Calhoun C, Tsai JC, Grunfield C, Feingold KR. Barrier disruption stimulates interleukin-1α expression and release from a pre-formed pool in murine epidermis. Journal of Investigative Dermatology 1996; 106:397-403.
  5. Zepter K, Häffner A, Soohoo LF, De Luca D, Tang HP, Fisher P, et al. Induction of biologically active IL-1 β-converting enzyme and mature IL-1β in human keratinocytes by inflammatory and immunologic stimuli. Journal of Immunology 1997; 159:6203-6208.
  6. Mauviel A, Heino J, Kähäri VM, Hartmann DJ, Loyau G, Pujol JP, et al. Comparative effects of interleukin-1 and tumor necrosis factor-α on collagen production and corresponding procollagen mRNA levels in human dermal fibroblasts. Journal of Investigative Dermatology 1991; 96:243-249.
  7. Mauviel A, Chen YQ, Kähäri VM, Ledo I, Wu M, Rudnicks L, et al. Human recombinant interleukin-1β up-regulates elastin gene expression in dermal fibroblasts. Journal of Biology Chemistry 1993; 268(9):6520-6524.
  8. Kupper TS. The activated keratinocyte: a model for inducible cytokine production by non-bone marrow- derived cells in cutaneous inflammatory and immune responses. Journal of Investigative Dermatology 1990; 94:146S-150S.
  9. Chen JD, Lapiere JC, Sauder DN, Peavey C, Woodley DT. Interleukin-1α stimulates keratinocyte migration through an epidermal growth factor/transforming growth factor-α-independent pathway. Journal of Investigative Dermatology 1995; 104:729-733.
  10. Pastar I, Stojadinovic O, Yin NC, Ramirez H, Nusbaum AG, Sawaya et al. Epithelialization in wound healing: A comprehensive review. Advances in Wound Care 2014; 3(7):445-464.
  11. Li W, Li Y, Guan S, Fan J, Cheng CF, Bright AM, et al. Extracellular heat shock protein-90α : linking hypoxia to skin cell motility and wound healing. EMBO Journal 2007; 26:1221-1233.
  12. Cheng CF, Fan J, Fedesco M, Guan S, Li Y, Bandyopadhyay B et al. Transforming growth factor alpha (TGF alpha)-stimulated secretion of HSP90alpha: using the receptor LRP-1/CD91 to promote human skin cell migration against a TGF beta-rich environment during wound healing. Molecular and Cellular Biology 2008; 28:3344-3358.
  13. Woodley DT, Fan J, Cheng CF, Li Y, Chen M, Bu G, et al. Participation of the lipoprotein receptor LRP1 in hypoxia-HSP90α autocrine signaling to promote keratinocyte migration. Journal of Cell Science 2009; 122:1495-1498.
  14. Georgopoulos, N and Dunnill, C. Skin Integrity Institute, University of Huddersfield. Pesonal communication.2016
  15. Zajicek R, Pafcuga I, Suca H, et al. Healing of widely meshed autografts using freshly isolated autologous epidermal cells and acellular Xe-Derma xenodermis. Hojeni ran 2012;6(2):12-18.
  16. Foster K, Richey K, Pressman M, Caruso D. Compassionate use of ReCell and meshed autografts in three patients with extensive burn injury. Presented at: The 47th Annual Meeting of the American Burn Association; 2015 Apr 21-24; Chicago, USA.
  17. Gravante G, Di Fede MC, Araco A, Grimaldi M, De Angelis B, Arpino A, Cervelli V, Montone A. A randomized trial comparing ReCell® system of epidermal cells delivery versus classic skin grafts for the treatment of deep partial thickness burns. Burns 2007; 33:966-972.
  18. Wood F, Martin L, Lewis D, Rawlins J, McWilliams T, Burrow S, Rea S. A prospective randomized clinical pilot study to compare the effectiveness of Biobrane® synthetic wound dressing, with or without autologous cell suspension, to the local standard treatment regimen in paediatric scald injuries. Burns 2012; 38:830-839.
  19. Komen L, Vrijman C, Tjin EP, Krebbers G, de Rie MA, Luiten RM, van der Veen J4, Wolkerstorfer A. Autologous cell suspension transplantation using a cell extraction device in segmental vitiligo and piebaldismpatients: A randomized controlled pilot study. J Am Acad Dermatol. 2015 Jul;73(1):170-2
  20. Billingham RE, Medawar PB. The technique of free skin grafting in mammals. Journal of Experimental Biology 1951; 385-402.
  21. Rheinwald JG, Green H. Serial cultivation of strains of human epidermal keratinocytes: the formation of keratinizing colonies from single cells. Cell 1975; 6(3):331-343.
  22. Navarro FA, Stoner ML, Lee HB, Park CS, Wood FM, Orgill DP. Melanocyte repopulation in full-thickness wounds using a cell spray apparatus. Journal of Burn Care and Research 2000; 22(1):41-46.
  23. Kwan P, Hori K, Ding J, Tredget EE (2009) Scar and contracture: biological principles. Hand Clin 25(4):511–28
  24. Sorrell JM, Caplan AI. Fibroblast heterogeneity: more than skin deep. J Cell Sci. 2004;117(Pt 5):667–675
  25. Grinnell F. Fibroblasts, myofibroblasts, and wound contraction. J Cell Biol. 1994, 124(4): 401-404