Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care | NextGen Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care Pipeline intelligence brief — engineered antifungal peptides for chronic wound biofilm infection, a significantly under-covered clinical challenge compared to bacterial biofilms. Published June 17, 2026 | Pipeline intelligence for wound care clinicians, product development teams, and wound-center medical directors Clinical Introduction Fungal biofilms are responsible for an estimated 1.6 million deaths annually worldwide, yet they receive a fraction of the R&D attention directed at bacterial biofilms. In chronic wound care, this disparity is consequential. Diabetic foot ulcers, venous stasis ulcers, and pressure injuries frequently harbor mixed bacterial-fungal biofilms where Candida albicans and Aspergillus species coexist with bacterial pathogens in a mutually protective extracellular matrix. The fungal component is regularly missed in clinical sampling, undertreated by standard antimicrobial protocols, and capable of driving persistent inflammation even when bacterial bioburden is controlled. This brief reviews the current state of antifungal peptide (AFP) research for biofilm disruption — a technology pipeline wound care product developers should track closely. Engineered AFPs represent a differentiated mechanism class: they penetrate biofilm matrices, disrupt fungal membrane integrity, and demonstrate synergy with conventional antifungals. With most antimicrobial peptide research fixed on bacterial targets, the antifungal gap is both a clinical blind spot and a technology market opportunity. Pipeline positioning: Antifungal peptide dressings are research-stage technologies. No FDA-cleared product currently exists for this indication. Preclinical research demonstrates biofilm-disrupting activity against Candida and Aspergillus species, but clinical efficacy and safety data remain limited. This brief is a competitive intelligence review, not a product recommendation. Why Fungal Biofilms Are Structurally Distinct and Clinically Undertreated Fungal biofilms differ from bacterial biofilms in clinically relevant ways. The extracellular matrix of Candida albicans biofilms contains high concentrations of β-glucan, mannan, and extracellular DNA — a denser, more mechanically robust barrier than most bacterial matrices. Fungal cells exhibit metabolic heterogeneity: surface cells are metabolically active while interior cells enter a drug-tolerant dormant state. Efflux pump overexpression, particularly Cdr1 and Cdr2 transporters, further reduces intracellular azole and echinocandin concentrations. In diabetic patients, already compromised immune function amplifies these vulnerabilities; preclinical research demonstrates that Candida biofilms in diabetic wound models persist longer and resist fluconazole and caspofungin more effectively than in nondiabetic models. Mixed biofilms — where Candida albicans coexists with Staphylococcus aureus or Pseudomonas aeruginosa — introduce an additional obstacle. Fungal hyphae provide a physical scaffold for bacterial adherence, and bacterial-fungal metabolic cross-feeding enhances antimicrobial tolerance for both organisms. Standard wound protocols that target only the bacterial component leave fungal reservoirs intact, facilitating biofilm regrowth and recurrent infection. Antifungal Peptide Mechanisms: Penetrate, Disrupt, Synergize Antifungal peptides are short, usually cationic amphipathic sequences that interact directly with fungal cell membranes and intracellular targets. Unlike small-molecule antifungals that inhibit specific biosynthetic enzymes (azole-CYP51, echinocandin-β-glucan synthase), AFPs act primarily through physical membrane disruption — a mechanism to which fungi have not developed widespread clinical resistance. The biofilm-relevant activities of engineered AFPs fall into three categories: Biofilm matrix penetration. Cationic AFPs bind to anionic components of the fungal matrix — β-glucan and extracellular DNA — facilitating diffusion through the biofilm where hydrophobic azoles cannot. Preclinical research demonstrates >80% penetration into mature Candida albicans biofilms within 30 minutes, compared to Membrane disruption and intracellular targeting. Upon reaching the fungal cell surface, AFPs form transmembrane pores or induce generalized membrane permeabilization, disrupting ion gradients and leading to osmotic lysis. Some AFPs also translocate intracellularly to bind mitochondrial DNA or ribosomal subunits, providing a second growth-inhibition mechanism. Synergy with conventional antifungals. Membrane permeabilization facilitates uptake of co-administered azoles and echinocandins. Checkerboard assays report fractional inhibitory concentration indices of 0.25–0.5 for AFP-azole combinations against fluconazole-resistant Candida albicans isolates — particularly relevant for wound care where biofilm tolerance drives treatment failure. It is important to note that these activities have been demonstrated primarily in vitro and in preclinical animal models. Clinical data on AFP efficacy in human wound infections are not yet available, and the translational gap between in vitro synergy and clinical biofilm eradication remains substantial. Mechanism AFP Action Clinical Relevance to Biofilm Biofilm matrix penetration Electrostatic binding to β-glucan and eDNA; diffusion through exopolymeric matrix. Addresses a key limitation of small-molecule antifungals (azole penetration failure). Membrane disruption Pore formation, ion gradient collapse, osmotic lysis. Physical mechanism with low expected resistance development. Intracellular targeting Mitochondrial DNA binding, ribosomal inhibition, nucleic acid synthesis disruption. Second mechanism for metabolically dormant biofilm subpopulations. Synergy with azoles/echinocandins Membrane permeabilization facilitates co-administered drug uptake. Potential to restore efficacy of frontline agents against resistant isolates. Design Strategies for Translational Viability Natural antimicrobial peptides — defensins, cathelicidins, histatins — provide the structural starting point for AFP engineering, but their clinical application is limited by serum protease susceptibility, off-target cytotoxicity, and high manufacturing costs. A June 2026 review (PMID 42231036) surveys the rational design strategies addressing these barriers: D-amino acid substitution. Replacing L-amino acids with D-enantiomers at protease-sensitive cleavage sites extends serum half-life from minutes to hours without compromising antifungal activity. D-enantiomer peptides retain membrane-disrupting capacity with significantly improved stability in wound exudate models. Lipidation. Conjugation of C12–C16 fatty acid chains enhances hydrophobic interaction with fungal membranes, improving Candida killing at lower concentrations. Chain length and saturation must be calibrated to avoid increased hemolytic activity. Cyclization. Head-to-tail or disulfide bridge cyclization constrains the peptide into a defined secondary structure that resists proteolytic unfolding. Cyclic AFPs maintain activity in serum for 6–12 hours compared to 30–60 minutes for linear counterparts and show superior activity against preformed biofilms. Nanoparticle delivery. Encapsulation into polymeric nanoparticles (PLGA, chitosan) or lipid nanocarriers enables controlled release over 7–14 days and protects the peptide from enzymatic degradation, aligning with weekly wound care visit schedules. Each strategy introduces trade-offs — cost, hemolytic potential, conformational rigidity, regulatory complexity — and the preclinical literature is converging on combinations (e.g., cyclic, lipidated D-enantiomer AFPs delivered via chitosan nanoparticle) as the most promising translational path. Development-stage note: The design strategies described above are drawn from preclinical research, primarily in vitro and murine wound model studies. One or more of these engineering approaches may eventually support a 510(k) submission if incorporated into a wound dressing device, but no AFP-based dressing has received FDA clearance or breakthrough device designation as of June 2026. Clinical timelines, manufacturing scale-up, and regulatory pathway remain uncertain. Market Gap and Strategic Implications The antimicrobial wound dressing market is dominated by bacterial-targeting technologies — silver, iodine, medical-grade honey, and more recently AMP-functionalized scaffolds. Most AMP research targets Staphylococcus aureus , Pseudomonas aeruginosa , and Acinetobacter baumannii . Fungal biofilm coverage is absent from virtually every commercial AMP dressing pipeline. This gap is not driven by low clinical need. PCR-based biofilm profiling detects fungal DNA in 30–60% of chronic wound specimens, and mixed bacterial-fungal biofilms are associated with longer healing times, higher amputation rates, and greater healthcare utilization compared to bacterial-only biofilms. Candida albicans is most frequently identified, but non-albicans Candida and Aspergillus species are increasingly recognized in wound cultures. A wound dressing with demonstrated antifungal biofilm activity — validated against Candida albicans and at least one Aspergillus species — would occupy a distinct competitive space. The regulatory pathway would likely be 510(k) clearance as a wound dressing with antimicrobial claims, supported by preclinical biofilm data and stability testing. However, no AFP dressing has reached the clinical trial stage for wound indications as of mid-2026. Serum stability, manufacturing scale of enantiomeric peptides, cytotoxicity optimization for repeated wound-bed application, and absence of validated clinical endpoints for antifungal wound-healing trials each represent material development hurdles. Key Takeaways Fungal biofilms contribute to an estimated 1.6 million deaths annually and are present in 30–60% of chronic wounds, yet remain under-recognized and undertreated in standard wound care protocols. Candida albicans and Aspergillus species form structurally distinct biofilms that resist conventional azole and echinocandin therapy through matrix density, metabolic heterogeneity, and efflux pump activity. Engineered AFPs address fungal biofilm infection through a physical membrane-disruption mechanism that penetrates biofilm matrices where small-molecule antifungals fail, and they demonstrate in vitro synergy with existing antifungal agents. Rational peptide design strategies — D-amino acid substitution, lipidation, cyclization, and nanoparticle delivery — are advancing AFP stability and translational viability in preclinical research. The antimicrobial wound dressing market has no current product with claimed antifungal biofilm activity, representing a differentiated pipeline opportunity for wound care product developers. All AFP technologies described are research-stage; no AFP-based wound dressing has received FDA clearance for clinical use as of June 2026. References Antifungal Peptides for Biofilm Disruption: Mechanisms, Design Strategies, and Translational Outlook. PubMed . 2026;PMID 42231036. Kuhn DM, Ghannoum MA. Candida biofilms: antifungal resistance and emerging therapeutic options. Curr Opin Investig Drugs. 2004;5(2):186-197. Ramage G, Mowat E, Jones B, Williams C, Lopez-Ribot J. Our current understanding of fungal biofilms. Crit Rev Microbiol. 2009;35(4):340-355. Nett JE, Andes DR. Fungal biofilms: in vivo models for discovery of anti-biofilm drugs. Microbiol Spectr. 2015;3(3):MB-0008-2014. Krom BP, Willems HM. Bacterial-fungal interactions in the wound microbiome: implications for chronic wound healing. Wound Repair Regen. 2022;30(2):145-156. Dowd SE, Delton Hanson J, Rees E, et al. Survey of fungi and yeast in polymicrobial infections in chronic wounds. J Wound Care. 2011;20(1):40-47. Harriott MM, Noverr MC. Importance of Candida-bacterial polymicrobial biofilms in disease. Trends Microbiol. 2011;19(11):557-563. Fernández L, Sol M, Upegui Y, et al. Antifungal peptide design strategies: from natural templates to engineered therapeutics. Adv Exp Med Biol. 2024;1446:97-122. Zhong G, Cheng J, Liang Z, et al. Short antifungal peptides with broad-spectrum activity against drug-resistant fungal pathogens. J Med Chem. 2023;66(12):8031-8046. Lohan S, Bisht GS. Recent approaches in combatting fungal infections: nanoparticle-based delivery systems. Int J Pharm. 2022;624:121997. Shurko JF, Galgiani JN, Ampel NM. Fungal biofilms and their clinical significance. Clin Microbiol Rev. 2020;33(4):e00019-20. Fong C, Acharya S, Sivamani RK, Rao JR. Polymicrobial biofilm in chronic wounds: a review. Wound Repair Regen. 2023;31(4):432-445. Lass-Flörl C. Current challenges in the diagnosis of fungal infections. Clin Microbiol Infect. 2023;29(7):847-851. Kuhn DM, George T, Chandra J, Mukherjee PK, Ghannoum MA. Antifungal susceptibility of Candida biofilms: unique efficacy of amphotericin B lipid formulations and echinocandins. Antimicrob Agents Chemother. 2002;46(6):1773-1780. Berkow EL, Lockhart SR, Ostrosky-Zeichner L. Antifungal susceptibility testing: current approaches. Clin Microbiol Rev. 2020;33(3):e00069-19. Bondaryk M, Kurzątkowski W, Staniszewska M. Antifungal agents commonly used in the superficial and mucosal candidiasis treatment: mode of action and resistance development. Postepy Dermatol Alergol. 2013;30(5):293-301. Sen S, Chakraborty R, De B. Amniotic membrane in biofilm-infected wounds: evidence and limitations. J Wound Care. 2022;31(Suppl 10):S12-S21. Disclaimer: This article is a pipeline intelligence review intended for healthcare professional and product development education. It does not constitute medical advice, treatment recommendation, or endorsement of any specific product or technology. Antifungal peptide wound dressings are research-stage technologies. No FDA-cleared product with antifungal biofilm claims currently exists for wound care indications. Clinical outcomes, regulatory clearance timelines, and commercial availability cannot be predicted from preclinical data. Individual patient results vary. Always verify current regulatory status, coding, and coverage before clinical adoption of any wound care technology. Track the Antimicrobial Peptide Pipeline NextGen Biologics monitors emerging wound care technologies for clinical and product development teams. Subscribe to our clinical briefs for intelligence on antimicrobial peptides, smart dressings, and biofilm-targeting platforms. Subscribe to Clinical Briefs at nextgenbiologicsusa.com

Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care | NextGen Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care Pipeline intelligence brief — en...

Published 2026-w25-antifungal | Clinical education for wound care physicians, podiatrists, nurses, and wound-center medical directors

Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care | NextGen Antifungal Peptide Biofilm Disruption: The Hidden Crisis in Chronic Wound Care Pipeline intelligence brief — engineered antifungal peptides for chronic wound biofilm infection, a significantly under-covered clinical challenge compared to bacterial biofilms. Published June 17, 2026 | Pipeline intelligence for wound care clinicians, product development teams, and wound-center medical directors Clinical Introduction Fungal biofilms are responsible for an estimated 1.6 million deaths annually worldwide, yet they receive a fraction of the R&D attention directed at bacterial biofilms. In chronic wound care, this disparity is consequential. Diabetic foot ulcers, venous stasis ulcers, and pressure injuries frequently harbor mixed bacterial-fungal biofilms where Candida albicans and Aspergillus species coexist with bacterial pathogens in a mutually protective extracellular matrix. The fungal component is regularly missed in clinical sampling, undertreated by standard antimicrobial protocols, and capable of driving persistent inflammation even when bacterial bioburden is controlled. This brief reviews the current state of antifungal peptide (AFP) research for biofilm disruption — a technology pipeline wound care product developers should track closely. Engineered AFPs represent a differentiated mechanism class: they penetrate biofilm matrices, disrupt fungal membrane integrity, and demonstrate synergy with conventional antifungals. With most antimicrobial peptide research fixed on bacterial targets, the antifungal gap is both a clinical blind spot and a technology market opportunity. Pipeline positioning: Antifungal peptide dressings are research-stage technologies. No FDA-cleared product currently exists for this indication. Preclinical research demonstrates biofilm-disrupting activity against Candida and Aspergillus species, but clinical efficacy and safety data remain limited. This brief is a competitive intelligence review, not a product recommendation. Why Fungal Biofilms Are Structurally Distinct and Clinically Undertreated Fungal biofilms differ from bacterial biofilms in clinically relevant ways. The extracellular matrix of Candida albicans biofilms contains high concentrations of β-glucan, mannan, and extracellular DNA — a denser, more mechanically robust barrier than most bacterial matrices. Fungal cells exhibit metabolic heterogeneity: surface cells are metabolically active while interior cells enter a drug-tolerant dormant state. Efflux pump overexpression, particularly Cdr1 and Cdr2 transporters, further reduces intracellular azole and echinocandin concentrations. In diabetic patients, already compromised immune function amplifies these vulnerabilities; preclinical research demonstrates that Candida biofilms in diabetic wound models persist longer and resist fluconazole and caspofungin more effectively than in nondiabetic models. Mixed biofilms — where Candida albicans coexists with Staphylococcus aureus or Pseudomonas aeruginosa — introduce an additional obstacle. Fungal hyphae provide a physical scaffold for bacterial adherence, and bacterial-fungal metabolic cross-feeding enhances antimicrobial tolerance for both organisms. Standard wound protocols that target only the bacterial component leave fungal reservoirs intact, facilitating biofilm regrowth and recurrent infection. Antifungal Peptide Mechanisms: Penetrate, Disrupt, Synergize Antifungal peptides are short, usually cationic amphipathic sequences that interact directly with fungal cell membranes and intracellular targets. Unlike small-molecule antifungals that inhibit specific biosynthetic enzymes (azole-CYP51, echinocandin-β-glucan synthase), AFPs act primarily through physical membrane disruption — a mechanism to which fungi have not developed widespread clinical resistance. The biofilm-relevant activities of engineered AFPs fall into three categories: Biofilm matrix penetration. Cationic AFPs bind to anionic components of the fungal matrix — β-glucan and extracellular DNA — facilitating diffusion through the biofilm where hydrophobic azoles cannot. Preclinical research demonstrates >80% penetration into mature Candida albicans biofilms within 30 minutes, compared to Membrane disruption and intracellular targeting. Upon reaching the fungal cell surface, AFPs form transmembrane pores or induce generalized membrane permeabilization, disrupting ion gradients and leading to osmotic lysis. Some AFPs also translocate intracellularly to bind mitochondrial DNA or ribosomal subunits, providing a second growth-inhibition mechanism. Synergy with conventional antifungals. Membrane permeabilization facilitates uptake of co-administered azoles and echinocandins. Checkerboard assays report fractional inhibitory concentration indices of 0.25–0.5 for AFP-azole combinations against fluconazole-resistant Candida albicans isolates — particularly relevant for wound care where biofilm tolerance drives treatment failure. It is important to note that these activities have been demonstrated primarily in vitro and in preclinical animal models. Clinical data on AFP efficacy in human wound infections are not yet available, and the translational gap between in vitro synergy and clinical biofilm eradication remains substantial. Mechanism AFP Action Clinical Relevance to Biofilm Biofilm matrix penetration Electrostatic binding to β-glucan and eDNA; diffusion through exopolymeric matrix. Addresses a key limitation of small-molecule antifungals (azole penetration failure). Membrane disruption Pore formation, ion gradient collapse, osmotic lysis. Physical mechanism with low expected resistance development. Intracellular targeting Mitochondrial DNA binding, ribosomal inhibition, nucleic acid synthesis disruption. Second mechanism for metabolically dormant biofilm subpopulations. Synergy with azoles/echinocandins Membrane permeabilization facilitates co-administered drug uptake. Potential to restore efficacy of frontline agents against resistant isolates. Design Strategies for Translational Viability Natural antimicrobial peptides — defensins, cathelicidins, histatins — provide the structural starting point for AFP engineering, but their clinical application is limited by serum protease susceptibility, off-target cytotoxicity, and high manufacturing costs. A June 2026 review (PMID 42231036) surveys the rational design strategies addressing these barriers: D-amino acid substitution. Replacing L-amino acids with D-enantiomers at protease-sensitive cleavage sites extends serum half-life from minutes to hours without compromising antifungal activity. D-enantiomer peptides retain membrane-disrupting capacity with significantly improved stability in wound exudate models. Lipidation. Conjugation of C12–C16 fatty acid chains enhances hydrophobic interaction with fungal membranes, improving Candida killing at lower concentrations. Chain length and saturation must be calibrated to avoid increased hemolytic activity. Cyclization. Head-to-tail or disulfide bridge cyclization constrains the peptide into a defined secondary structure that resists proteolytic unfolding. Cyclic AFPs maintain activity in serum for 6–12 hours compared to 30–60 minutes for linear counterparts and show superior activity against preformed biofilms. Nanoparticle delivery. Encapsulation into polymeric nanoparticles (PLGA, chitosan) or lipid nanocarriers enables controlled release over 7–14 days and protects the peptide from enzymatic degradation, aligning with weekly wound care visit schedules. Each strategy introduces trade-offs — cost, hemolytic potential, conformational rigidity, regulatory complexity — and the preclinical literature is converging on combinations (e.g., cyclic, lipidated D-enantiomer AFPs delivered via chitosan nanoparticle) as the most promising translational path. Development-stage note: The design strategies described above are drawn from preclinical research, primarily in vitro and murine wound model studies. One or more of these engineering approaches may eventually support a 510(k) submission if incorporated into a wound dressing device, but no AFP-based dressing has received FDA clearance or breakthrough device designation as of June 2026. Clinical timelines, manufacturing scale-up, and regulatory pathway remain uncertain. Market Gap and Strategic Implications The antimicrobial wound dressing market is dominated by bacterial-targeting technologies — silver, iodine, medical-grade honey, and more recently AMP-functionalized scaffolds. Most AMP research targets Staphylococcus aureus , Pseudomonas aeruginosa , and Acinetobacter baumannii . Fungal biofilm coverage is absent from virtually every commercial AMP dressing pipeline. This gap is not driven by low clinical need. PCR-based biofilm profiling detects fungal DNA in 30–60% of chronic wound specimens, and mixed bacterial-fungal biofilms are associated with longer healing times, higher amputation rates, and greater healthcare utilization compared to bacterial-only biofilms. Candida albicans is most frequently identified, but non-albicans Candida and Aspergillus species are increasingly recognized in wound cultures. A wound dressing with demonstrated antifungal biofilm activity — validated against Candida albicans and at least one Aspergillus species — would occupy a distinct competitive space. The regulatory pathway would likely be 510(k) clearance as a wound dressing with antimicrobial claims, supported by preclinical biofilm data and stability testing. However, no AFP dressing has reached the clinical trial stage for wound indications as of mid-2026. Serum stability, manufacturing scale of enantiomeric peptides, cytotoxicity optimization for repeated wound-bed application, and absence of validated clinical endpoints for antifungal wound-healing trials each represent material development hurdles. Key Takeaways Fungal biofilms contribute to an estimated 1.6 million deaths annually and are present in 30–60% of chronic wounds, yet remain under-recognized and undertreated in standard wound care protocols. Candida albicans and Aspergillus species form structurally distinct biofilms that resist conventional azole and echinocandin therapy through matrix density, metabolic heterogeneity, and efflux pump activity. Engineered AFPs address fungal biofilm infection through a physical membrane-disruption mechanism that penetrates biofilm matrices where small-molecule antifungals fail, and they demonstrate in vitro synergy with existing antifungal agents. Rational peptide design strategies — D-amino acid substitution, lipidation, cyclization, and nanoparticle delivery — are advancing AFP stability and translational viability in preclinical research. The antimicrobial wound dressing market has no current product with claimed antifungal biofilm activity, representing a differentiated pipeline opportunity for wound care product developers. All AFP technologies described are research-stage; no AFP-based wound dressing has received FDA clearance for clinical use as of June 2026. References Antifungal Peptides for Biofilm Disruption: Mechanisms, Design Strategies, and Translational Outlook. PubMed . 2026;PMID 42231036. Kuhn DM, Ghannoum MA. Candida biofilms: antifungal resistance and emerging therapeutic options. Curr Opin Investig Drugs. 2004;5(2):186-197. Ramage G, Mowat E, Jones B, Williams C, Lopez-Ribot J. Our current understanding of fungal biofilms. Crit Rev Microbiol. 2009;35(4):340-355. Nett JE, Andes DR. Fungal biofilms: in vivo models for discovery of anti-biofilm drugs. Microbiol Spectr. 2015;3(3):MB-0008-2014. Krom BP, Willems HM. Bacterial-fungal interactions in the wound microbiome: implications for chronic wound healing. Wound Repair Regen. 2022;30(2):145-156. Dowd SE, Delton Hanson J, Rees E, et al. Survey of fungi and yeast in polymicrobial infections in chronic wounds. J Wound Care. 2011;20(1):40-47. Harriott MM, Noverr MC. Importance of Candida-bacterial polymicrobial biofilms in disease. Trends Microbiol. 2011;19(11):557-563. Fernández L, Sol M, Upegui Y, et al. Antifungal peptide design strategies: from natural templates to engineered therapeutics. Adv Exp Med Biol. 2024;1446:97-122. Zhong G, Cheng J, Liang Z, et al. Short antifungal peptides with broad-spectrum activity against drug-resistant fungal pathogens. J Med Chem. 2023;66(12):8031-8046. Lohan S, Bisht GS. Recent approaches in combatting fungal infections: nanoparticle-based delivery systems. Int J Pharm. 2022;624:121997. Shurko JF, Galgiani JN, Ampel NM. Fungal biofilms and their clinical significance. Clin Microbiol Rev. 2020;33(4):e00019-20. Fong C, Acharya S, Sivamani RK, Rao JR. Polymicrobial biofilm in chronic wounds: a review. Wound Repair Regen. 2023;31(4):432-445. Lass-Flörl C. Current challenges in the diagnosis of fungal infections. Clin Microbiol Infect. 2023;29(7):847-851. Kuhn DM, George T, Chandra J, Mukherjee PK, Ghannoum MA. Antifungal susceptibility of Candida biofilms: unique efficacy of amphotericin B lipid formulations and echinocandins. Antimicrob Agents Chemother. 2002;46(6):1773-1780. Berkow EL, Lockhart SR, Ostrosky-Zeichner L. Antifungal susceptibility testing: current approaches. Clin Microbiol Rev. 2020;33(3):e00069-19. Bondaryk M, Kurzątkowski W, Staniszewska M. Antifungal agents commonly used in the superficial and mucosal candidiasis treatment: mode of action and resistance development. Postepy Dermatol Alergol. 2013;30(5):293-301. Sen S, Chakraborty R, De B. Amniotic membrane in biofilm-infected wounds: evidence and limitations. J Wound Care. 2022;31(Suppl 10):S12-S21. Disclaimer: This article is a pipeline intelligence review intended for healthcare professional and product development education. It does not constitute medical advice, treatment recommendation, or endorsement of any specific product or technology. Antifungal peptide wound dressings are research-stage technologies. No FDA-cleared product with antifungal biofilm claims currently exists for wound care indications. Clinical outcomes, regulatory clearance timelines, and commercial availability cannot be predicted from preclinical data. Individual patient results vary. Always verify current regulatory status, coding, and coverage before clinical adoption of any wound care technology. Track the Antimicrobial Peptide Pipeline NextGen Biologics monitors emerging wound care technologies for clinical and product development teams. Subscribe to our clinical briefs for intelligence on antimicrobial peptides, smart dressings, and biofilm-targeting platforms. Subscribe to Clinical Briefs at nextgenbiologicsusa.com