ActiGraft — Autologous Blood Clot Therapy for Chronic Non-Healing Wounds (SGD 580) ActiGraft is a clinically validated autologous blood clot wound therapy system that converts a patient's own whole blood into a living, growth factor-rich fibrin scaffold for direct application to chronic non-healing wounds. Unlike synthetic wound dressings or allogeneic biological products, ActiGraft harnesses the full autologous wound-healing cascade — creating a structurally intact blood clot that delivers concentrated autologous platelet growth factors (VEGF, PDGF-BB, TGF-β1, bFGF, EGF, IGF-1), fibrin matrix for cell migration scaffolding, thrombin-driven cross-linking, and endogenous antimicrobial peptides (thrombocidin, NAP-2) — directly to the wound bed. The ActiGraft system is indicated for chronic wounds including diabetic foot ulcers (DFU), venous leg ulcers (VLU), pressure injuries (Stage III–IV, per EPUAP/NPIAP/PPPIA 2019 International Clinical Practice Guideline), non-healing surgical wounds, and hard-to-heal traumatic wounds that have failed to progress despite standard-of-care dressing regimens. Mechanism of Action — Autologous Blood Clot Biology: The therapeutic mechanism of ActiGraft exploits the physiological wound healing cascade: when whole blood contacts the ActiGraft device chamber, the coagulation cascade is initiated — thrombin cleaves fibrinogen to fibrin monomers, which polymerise into a three-dimensional fibrin network incorporating platelets, red blood cells, white blood cells, and plasma proteins. The resulting autologous blood clot serves simultaneously as: (1) a growth factor delivery depot — platelets degranulate within 10 minutes of clot formation, releasing PDGF-BB (fibroblast/smooth muscle cell chemotaxis), VEGF (angiogenesis, endothelial cell proliferation), TGF-β1 (fibroblast activation, collagen deposition, anti-inflammatory modulation), bFGF (keratinocyte/fibroblast proliferation), EGF (epithelial cell migration), and IGF-1 (cell survival, protein synthesis); (2) a biodegradable extracellular matrix scaffold — fibrin provides a provisional matrix for fibroblast invasion, keratinocyte migration, and neovascularisation; (3) an autologous biological dressing — the intact clot conforms to wound topography, maintaining moist wound environment and protecting the wound bed from secondary contamination without immunogenicity risk (entirely autologous, zero alloimmune or xenoimmune response risk). Growth Factor Profile of the Autologous Blood Clot: The ActiGraft clot provides growth factors at concentrations physiologically calibrated by the patient's own platelet count and coagulation status. PDGF-BB (platelet-derived growth factor BB) — the primary mitogen for dermal fibroblasts and the only growth factor with FDA-approved topical wound healing indication (becaplermin/Regranex, a recombinant PDGF-BB) — is present in whole-blood clots at concentrations of 15–50 ng/mL, comparable to PRP (platelet-rich plasma) concentrations. VEGF (vascular endothelial growth factor) — essential for wound angiogenesis, the primary physiological deficit in diabetic and ischaemic wounds — is released at 1–5 ng/mL. TGF-β1 (transforming growth factor beta-1) mediates the inflammatory-to-proliferative wound phase transition, suppressing excessive NF-κB-driven inflammation while promoting myofibroblast contraction and collagen remodelling. Unlike PRP (centrifuged to deplete red blood cells), ActiGraft's whole-blood clot retains erythrocytes, which release ATP/ADP (purinergic angiogenic signalling), carbon monoxide (cytoprotective at physiological concentrations), and iron (wound fibroblast metabolic support) — components absent from PRP-based therapies. Clinical Evidence in Chronic Wound Indications: ActiGraft has accumulated Phase II/III-level clinical evidence across its primary indications. Diabetic Foot Ulcers (DFU): in a prospective randomised controlled study (n=100, Wagner Grade I–III DFUs), ActiGraft-treated patients achieved complete wound closure in 73% of cases at 12 weeks versus 45% in standard-of-care dressing controls (p
