Three platforms.
One wound healing cascade.
Antimicrobial matrices, human placental allografts, and collagen dressing systems — each targeting distinct failure points in the chronic wound proteolytic cascade.
Three platforms. Each targets a distinct failure point.
Chronic wounds stall in a self-amplifying proteolytic cycle. Each of our three platforms addresses a different driver — together, they reset the cascade.
Collagen Dressings
Sacrificial substrate sequesters excess MMPs. Restores protease : anti-protease balance. Enables inflammation → proliferation phase transition.
Microlyte SAM
Sub-cytotoxic silver breaks the biofilm cycle. Bioresorbable scaffold supports granulation. No removal trauma.
Amniotic Membrane
Multi-layer biological pharmacy: 25+ growth factors, HC-HA/PTX3 complex, native ECM scaffold.
Why chronic wounds fail to heal.
Chronic wounds are locked in a self-amplifying proteolytic cycle. MMPs at 30× physiological levels destroy growth factors, native ECM, and their own inhibitors. Biofilm maintains inflammation. Senescent fibroblasts amplify the cascade.
MMP Overexpression
MMP-9 in poor healers: 17× higher. PDGF degraded within 2 hours.
Biofilm Persistence
60–90% of chronic wounds. EPS matrix shields bacteria from immunity.
Growth Factor Sink
Proteolytic environment degrades growth factors before signaling can occur.
Cellular Senescence
>15% senescent cells = treatment-resistant. SASP amplifies MMPs.
Sequential cascade reset
Collagen Dressings
Sacrificial substrate sequesters excess MMPs. Restores protease : anti-protease balance.
Microlyte SAM
Sub-cytotoxic silver breaks biofilm cycle. Bioresorbable scaffold supports granulation.
Amniotic Membrane
25+ growth factors, HC-HA/PTX3 complex, native ECM scaffold.
Amniotic membrane — layer architecture.
Over 25 growth factors, anti-inflammatory cytokines, and TIMPs in native ECM. Each layer contributes distinct biology to wound healing.
Amnion
Basement membrane: Type IV Collagen, Laminin-1/5, Fibronectin
Growth factors: EGF, FGF-2, PDGF-AA/BB, VEGF, KGF, HGF, TGF-α, IGF-1
Anti-inflammatory: HC-HA/PTX3, IL-10, IL-1Ra, PGE2, TIMP-1/2/3/4
Intermediate (Spongy) Layer
Composition: HA >4,000 kDa · Type III Collagen · Decorin · Biglycan · Proteoglycans
Function: Growth factor reservoir · anti-fibrotic TGF-β sequestration via decorin
Chorion
Collagen matrix: Types I, III, IV, V, VI · Fibronectin · Tenascin
Structure: Dense reticular network · trophoblast growth factor production
Function: Mechanical backbone · slow-diffusion sustained release
HC-HA/PTX3 anti-inflammatory master switch
HA >4,000 kDa + heavy chain 1 via TSG-6 + pentraxin 3 drives apoptosis of activated neutrophils/macrophages, M2 polarization, and Treg expansion. Downregulates TGF-β1 mRNA + receptors I/II/III and activates BMP — reverting myofibroblasts and attenuating nociceptive excitability.
Membrane Wrap Lite
Basement-membrane scaffold + growth-factor monolayer. Cost-effective entry point.
Membrane Wrap
2× ECM + growth-factor payload. Enhanced structural integrity and sustained GF kinetics.
Tri-Membrane Wrap
A-C-A sandwich: highest ECM concentration. Dense chorion collagen between two amnion layers. Escalation product.
Microlyte® SAM™ — sub-cytotoxic silver.
PEM nanofilm on bioresorbable PVA. 50–100× less silver than conventional dressings. Equivalent 99.99% antimicrobial kill via intimate surface-contact delivery.
Conventional Dressing
Cytotoxic to fibroblasts & keratinocytes
Microlyte SAM
99.99% kill · 72+ hrs · bioresorbable 7 days
Polymer science
PEM nanofilm architecture
Layer-by-layer cationic/anionic polymer assembly. Cationic termination enhances cell attachment, ECM production, and actin organization via electrostatic interaction with proteoglycans.
PVA cytophilicity
Hydroxyl (–OH) groups hydrogen-bond with ECM proteins (fibronectin, vitronectin). Presents integrin-binding domains. Mechanical properties mimic native soft tissue.
Bioresorbable design
~20 µm PVA resorbs in 7 days. No removal → no granulation disruption. Integrates without foreign-body response. 4-year shelf life.
Type I Collagen — sacrificial substrate & bioactive signal.
Exogenous collagen reverses the proteolytic cycle by diverting MMP activity from endogenous ECM. As it degrades, it releases bioactive matrikines that actively drive granulation and fibroblast chemotaxis.
Chronic Wound
MMPs: 30× physiologic · GFs: degraded · ECM: destroyed · TIMPs: gone. Self-amplifying cycle.
Exogenous Collagen
Sacrificial MMP substrate. Diverts proteases from native ECM. Restores MMP : TIMP ratio.
Healing Wound
Phase transition enabled. GFs preserved · ECM intact. Proliferation phase initiated.
GHK-Cu tripeptide
Promotes collagen synthesis · upregulates VEGF & bFGF expression.
RGD sequences (exposed via MMP)
Integrin α1β1, α2β1 binding · fibroblast chemotaxis.
α11β1 by day 7: granulation + tensile strength · DDR1/2 → β1-integrin & α-SMA
Clinical evidence — two pathways
Reimbursable during the global surgical period.
Full-thickness or wounds stalled >4 weeks.
Product selection by wound presentation.
Matching the right platform to the dominant failure mode of the wound in front of you.
| Wound Presentation | Primary Product | Mechanism | Key Evidence |
|---|---|---|---|
| Post-op surgical incision | Collagen dressing | Sacrificial MMP substrate, hemostasis, SSI prevention | 59% SSI reduction (n = 5,335) |
| Active biofilm / infection risk | Microlyte SAM (A2005) | Sub-cytotoxic ionic silver, 99.99% kill, 72+ hrs | 91% healed or improved at 12 wk |
| Shallow / early chronic | Membrane Wrap Lite | Single-amnion barrier, ECM scaffold, GF delivery | BM re-epithelialization template |
| Standard DFU / VLU | Membrane Wrap (Dual-layer) | 2× ECM payload, structural persistence | Sustained GF, dual-layer kinetics |
| Recalcitrant / failed grafts | Tri-Membrane Wrap (A-C-A) | Highest ECM concentration, chorion sandwich | Escalation — max biological payload |
CheckMyWoundCareNotes.com
Automated compliance review against LCD L35041, A54117, MPIM 3.6.2.2, SSA 1862(a)(1)(A). Pre-submission gap detection, FPS pattern flagging, and corrective-language generation.
Pre-submission review
Upload notes → automated check against LCD criteria, documentation requirements, and frequency limits.
FPS pattern detection
Flags cloned documentation, utilization outliers, wastage patterns, and product-selection anomalies.
Corrective language
LCD-aligned clinical prose generated from documented findings. Audit-defensible.
The only wound care partner delivering product + compliance + science in a single relationship.
Go deeper with our clinical team.
Schedule a scientific review — we'll walk your team through each platform, LCD alignment, and the evidence base for the wounds you see most.