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Elafin

Tier 1 · Human trials
Also known as Peptidase inhibitor 3 · Trappin-2 · SKALP

The strongest evidence is Tier 1: a completed 87-patient randomised placebo-controlled CABG trial (8/7/8) and a completed Phase I single-dose escalating safety study, plus an EU-registered Phase I trial (NCT03522935). However, most disease-specific evidence (gut, HIV/HSV, cartilage, systemic sclerosis, hidradenitis suppurativa, lichen planus, reproductive tract) is observational, in vitro or animal. The pivotal CABG trial missed its primary endpoint despite strong biomarker effects. Half-life quantification, the 75-patient combined safety claim and orphan designations come from single/vendor/developer sources; general peptide context comes from a tier-3 preprint. Elafin is not approved for human therapeutic use.

Half-life
~6 h
Routes
Subcutaneous · Intravenous · Topical
Goals
Anti-inflammatory · Tissue protection / repair · Antimicrobial / antiviral · Cardiovascular / ischaemia-reperfusion protection
Cost / mg
Not recorded

How it works

Elafin (also called Trappin-2 or SKALP) is described by DrugBank as a human protein made naturally in the skin, lung and breast that protects tissue from destruction by the immune system and blocks destructive enzymes involved in inflammation. A vendor profile and reviews describe it as an endogenous serine protease inhibitor produced by epithelial cells at mucosal surfaces that blocks neutrophil enzymes (elastase and proteinase 3) and also has direct antimicrobial activity against bacteria and fungi(vendor claim). Because the enzyme elastase is increased in pulmonary hypertension and inflammatory tissue damage, researchers have investigated giving extra elafin to dampen this damage. In its most rigorous human test — a randomised trial in heart-bypass surgery patients — elafin dramatically raised blood elafin levels and inhibited elastase but did not reduce heart-muscle injury over 48 hours.

Overview

Overview

Elafin (also known as Peptidase inhibitor 3, Trappin-2 and SKALP; INN Tiprelestat) is an endogenous human protein under investigation as a therapeutic. DrugBank describes it as a human protein produced naturally in the skin, lung and breast that protects tissue from destruction by the immune system and blocks the activity of destructive enzymes involved in inflammatory reactions. A vendor profile characterizes it as an endogenous serine protease inhibitor peptide produced by epithelial cells at mucosal surfaces that inhibits neutrophil elastase and proteinase 3 and exhibits direct antimicrobial activity against bacteria and fungi(vendor claim). Although some sources describe it as 'serpin-like', this is inaccurate: elafin belongs to the WAP (whey acidic protein) four-disulfide-core family of inhibitors and blocks its target proteases by a competitive tight-binding mechanism, which is distinct from the irreversible suicide-substrate trap used by true serpins. A review4 describes its structure as an N-terminal transglutaminase substrate motif and a C-terminal WAP (whey acidic protein) domain, and reports it inhibits neutrophil elastase and proteinase-3 by a competitive tight-binding mechanism.

It is not approved for human therapeutic use. Sources indicate it remains investigational; a vendor profile explicitly states it is not approved, and one EU registration notes it had no marketing authorization and was not designated an orphan drug at that time(vendor claim).

Development status

  • A vendor profile reports elafin is at the Phase II clinical trials stage (with 31 studies noted)(vendor claim). A review4 notes it was well tolerated in a Phase I clinical trial and that Phase II trials were underway on post-operative inflammation, focusing on reduction of post-operative morbidity after oesophagus cancer surgery, coronary artery bypass surgery and kidney transplantation.
  • A Phase I trial (NCT03522935) planned subcutaneous daily administration for 7 days in normal healthy subjects, followed over 28 days, across 5 groups of 6 subjects (30 total) at 0.03, 0.06, 0.10, 0.15 and 0.18 mg/kg, running 2019–2020. The trial states elafin inhibits elastase, an enzyme increased in pulmonary hypertension and a major factor in the development of PAH, and that elafin is being developed for treatment of PAH.
  • The developer Tiakis reports elafin (Tiprelestat), identical to the human protein, entered a Phase I trial with Duke University's Early Phase Research Unit for subcutaneous use assessing safety and tolerability of repeated single doses in healthy individuals.

Cardiac / CABG evidence

An EU-registered randomised controlled trial evaluated whether perioperative elafin infusion reduces post-ischaemic inflammatory myocardial injury following coronary artery bypass graft (CABG) surgery, enrolling 87 subjects in the UK. In that single-centre trial, 87 patients were randomised 1:1 to intravenous elafin 200 mg or saline placebo after induction of anaesthesia and prior to sternotomy. The trial authors describe elafin as a potent endogenous neutrophil elastase inhibitor that protects against myocardial inflammation and injury in preclinical models of ischaemia-reperfusion injury. Infusion was safe and produced a >3000-fold increase in plasma elafin and >50% inhibition of elastase activity in the first 24 hours. However, elafin did not reduce myocardial injury over 48 hours (ratio of geometric means AUC troponin I 0.74, 95% CI 0.47–1.15, p=0.18), had no effect on myocardial infarction (7/34 vs 5/35) nor on inflammation markers (hs-CRP p=0.16; MPO p=0.320). A post hoc analysis of the high-sensitive assay found lower troponin I at 6 hours in elafin-treated patients (median 2.4 vs 4.1 μg/L, p=0.035). The trial authors concluded there was no strong evidence that single-dose elafin reduced myocardial injury and inflammation following CABG-induced ischaemia-reperfusion injury. Note that developer (Tiakis) material describes CABG treatment as producing 'postoperative reduction of troponin I' — a more favourable framing than the trial's null primary result.

Other reported research directions

  • Pulmonary hypertension: Tiakis reports that in PAH models elafin reverses obliterative changes in arteries of lung explants from PAH patients and leads to regression of pulmonary vascular lesions in rats, and that elafin has received orphan drug designations in the USA and EU for PAH (developer-reported). A study17 reports neutrophil extracellular vesicles from PAH patient plasma induced pulmonary hypertension in mice, an effect mitigated by elafin.
  • Gut/inflammatory bowel: Reviews describe trappin-2/elafin contributing to the mucosal shield against luminal microbes and report accumulating evidence of protective effects in gut disorders and gluten sensitization, considering therapeutic potential of mucosal delivery.
  • Antimicrobial/antiviral: In vitro studies report recombinant trappin-2/elafin inhibits HIV-1 (elafin ~130× more potent than trappin-2) and HSV-2 (elafin ~7× more potent), inhibits HIV-1 attachment and transcytosis, and that a transgenic mouse study found reduced HSV-2 viral load in the CNS. A mouse study found elafin active against Pseudomonas aeruginosa via adenovirus-mediated gene transfer.
  • Skin: A study describes elafin as absent in normal skin but highly expressed in inflamed skin keratinocytes, with overexpression reported in cellulitis, psoriasis, Behçet's syndrome and graft versus host disease. Serum elafin was significantly higher in lichen planus patients than controls (32.56 vs 5.60 ng/mL, p<0.001). SKALP/elafin mRNA was significantly elevated in lesional hidradenitis suppurativa skin.
  • Other: Observational studies report elevated trappin-2 in osteoarthritis cartilage and correlations with renal dysfunction and pulmonary pressure in systemic sclerosis; a reproductive-tract study found elafin diminished with bacterial vaginosis.

Most of this disease-specific evidence is in vitro, animal or observational; human efficacy in these indications has not been established. A tier-3 preprint review provides general context on peptide drugs, projecting global sales of approved peptide drugs to reach ~$75 billion by 2028 and warning of a gray market of unapproved peptides sold direct-to-consumer.

What the research shows

203 findings extracted from the 27 sources cited below, strongest evidence first within each group. Every one links to the source it came from.

What human studies found

Based on 16 human trial findings, 26 human study findings, 5 animal findings, 1 in vitro finding and 2 expert opinion findings.

  • human trialA placebo-controlled randomized trial evaluated the effect of elafin on cytokine profiles after major surgery in a Phase II trial1

  • human trialStudy was single center and performed with approval of national research ethics committee and MHRA2

  • human trialElafin (INN: Tiprelestat) entered Phase I clinical trial for subcutaneous use assessing safety and tolerability of repeated single doses in healthy individuals5

  • human trialElafin did not reduce myocardial injury over 48 h (ratio of geometric means (elafin/placebo) of AUC troponin I 0.74 (95% CI 0.47 to 1.15, p=0.18))7

  • human trialPost hoc analysis of the high-sensitive assay revealed lower troponin I concentrations at 6 h in elafin-treated patients (median 2.4 vs 4.1 μg/L, p=0.035)7

  • human trialElafin had no effect on myocardial infarction (elafin, 7/34 vs placebo, 5/35 patients)7

  • human trialElafin had no effect on markers of inflammation: mean differences for AUC hs-CRP of 499 mg/L/48 h (95% CI -207 to 1205, p=0.16), and AUC MPO of 238 ng/mL/48 h (95% CI -235 to 711, p=0.320)7

  • human trialElafin did not reduce myocardial injury over 48 h (ratio of geometric means (elafin/placebo) of AUC troponin I 0.74 (95% CI 0.47 to 1.15, p=0.18))8

Show 42 more findings

  • human trialPost hoc analysis of the high-sensitive assay revealed lower troponin I concentrations at 6 h in elafin-treated patients (median 2.4 vs 4.1 μg/L, p=0.035)8

  • human trialElafin had no effect on myocardial infarction (elafin, 7/34 vs placebo, 5/35 patients)8

  • human trialElafin had no effect on markers of inflammation: mean differences for AUC hs-CRP of 499 mg/L/48 h (95% CI -207 to 1205, p=0.16), and AUC MPO of 238 ng/mL/48 h (95% CI -235 to 711, p=0.320)8

  • human trialElafin did not reduce myocardial injury over 48 h (ratio of geometric means (elafin/placebo) of AUC troponin I 0.74 (95% CI 0.47 to 1.15, p=0.18))9

  • human trialPost hoc analysis of the high-sensitive assay revealed lower troponin I concentrations at 6 h in elafin-treated patients (median 2.4 vs 4.1 μg/L, p=0.035)9

  • human trialElafin had no effect on myocardial infarction (elafin, 7/34 vs placebo, 5/35 patients)9

  • human trialElafin had no effect on markers of inflammation: mean differences for AUC hs-CRP of 499 mg/L/48 h (95% CI -207 to 1205, p=0.16), and AUC MPO of 238 ng/mL/48 h (95% CI -235 to 711, p=0.320)9

  • human trialThere was no strong evidence that neutrophil elastase inhibition with a single-dose elafin treatment reduced myocardial injury and inflammation following CABG-induced ischaemia-reperfusion injury9

  • human studyTreatment of patients undergoing esophageal cancer surgery resulted in significantly shorter intensive care unit stay and positive postoperative effect on liver and kidney markers5

  • human studyTreatment of patients undergoing coronary artery bypass surgery resulted in postoperative reduction of the heart damage marker troponin I5

  • human studyOverexpression of Elafin has been reported in various infective, inflammatory skin disorders, such as cellulitis, psoriasis, Behçet's syndrome, and graft versus host disease6

  • human studySerum Elafin level was significantly higher in LP patients as compared to healthy controls6

  • human studySLPI and elafin are often inactivated in inflammatory secretions in patients with chronic pathologies in the lung and elsewhere10

  • human studyAntiprotease supplementation with SLPI/elafin in clinical protocols has demonstrated proof of principle10

  • human studyElafin was found in all 112 samples of cervicovaginal secretions11

  • human studyElafin levels were diminished in women with bacterial vaginosis11

  • human studyElafin is a component of cervicovaginal secretions in pregnancy11

  • human studyTrappin-2 was detectable in OA articular cartilage extracts, cultured chondrocytes, conditioned media, and SF by Western blotting12

  • human studyOA cartilage protein extracts contained significantly higher quantities of trappin-2 than normal cartilage protein extracts12

  • human studyImmunohistochemical studies of OA cartilage revealed trappin-2 protein in chondrocytes12

  • human studyExpression of trappin-2/elafin is differentially regulated in diseases associated with gut inflammation13

  • human studyTrappin-2/elafin has protective effects in gut intestinal disorders associated with acute or chronic inflammation13

  • human studyTrappin-2/elafin has protective effects in gluten sensitization disorders13

  • human studyNeutrophils from patients with pulmonary arterial hypertension produce and release increased neutrophil elastase, associated with enhanced extracellular traps17

  • human studySKALP/elafin mRNA expression is significantly elevated in lesional compared with nonlesional skin of hidradenitis suppurativa patients18

  • human studySerum trappin-2 levels inversely correlated with estimated glomerular filtration rate in SSc patients with renal dysfunction19

  • human studySerum trappin-2 levels were significantly increased in SSc patients with digital ulcers or elevated RVSP compared to those without19

  • human studySerum trappin-2 levels positively correlated with RVSP values in SSc patients19

  • human studyPrevalence of digital ulcers or elevated right ventricular systolic pressure (RVSP) was significantly higher in SSc patients with elevated serum trappin-2 levels than in those with normal levels19

  • human studyTrappin-2 expression was enhanced in small vessels of SSc lesional skin19

  • human studyEndothelial trappin-2 up-regulation partially due to Fli1 deficiency can be associated with the development of SSc vasculopathy19

  • human studyTr/E are among principal anti-HIV-1 molecules in cervicovaginal lavage (CVL) fluid20

  • human studyAverage levels of secreted Trappin-2/Elafin were higher in cervico-vaginal lavages from HIV-negative women compared to HIV-positive women, although values did not reach statistical significance23

  • human studyWomen at the secretory phase of the menstrual cycle produced more Trappin-2/Elafin in cervico-vaginal lavages relative to women at the proliferative phase23

  • animalStudies on several animal models show that antiprotease augmentation with human elafin is an effective strategy in the treatment of inflammatory vascular, systemic and pulmonary diseases4

  • animalStudies on several animal models show that antiprotease augmentation with human elafin is an effective strategy in treatment of inflammation triggered by reperfusion injury4

  • animalTreatment with Elafin leads to regression of pulmonary vascular lesions in rats5

  • animalTrappin-2/Elafin linked to susceptibility or protection against inflammatory disease and infections21

  • animalElafin is active against Pseudomonas aeruginosa infection in mice in vivo using an adenovirus-mediated gene transfer overexpression strategy26

  • in vitroRecombinant Trappin-2/Elafin was able to inhibit both T-cell-tropic X4/IIIB and macrophage-tropic R5/BaL HIV-1 in a dose-dependent manner23

  • expert opinionAccumulating evidence has demonstrated the protective effects of trappin-2/elafin in gut intestinal disorders associated with acute or chronic inflammation, or with gluten sensitization disorders13

  • expert opinionApproved peptide drugs undergo a rigorous path of development and approval, with extensive clinical trials often consisting of thousands of subjects to establish efficacy and safety27

How it works

Based on 2 human trial findings, 22 human study findings, 4 animal findings, 59 in vitro findings, 18 expert opinion findings and 5 theoretical findings.

  • human trialElafin resulted in >50% inhibition of elastase activity in the first 24 h7

  • human trialElafin resulted in >50% inhibition of elastase activity in the first 24 h8

  • human studyElafin could be part of the inflammatory autoimmune process in LP6

  • human studyElafin and secretory leukocyte protease inhibitor (SLPI) are pleiotropic molecules chiefly synthesized at the mucosal surface10

  • human studyElafin and SLPI have a fundamental role in the surveillance against microbial infections10

  • human studyElafin functions as an anti-protease in the inflammatory milieu10

  • human studyElafin has antimicrobial function10

  • human studyElafin modulates innate and adaptive immunity10

Show 102 more findings

  • human studyElafin regulates tissue repair10

  • human studyInactivation of SLPI and elafin occurs through the action of host or microbial products10

  • human studyElafin is expressed in the cervical glandular epithelium11

  • human studyElafin may be an important component of innate immunity in the lower genital tract11

  • human studyTrappin-2 is present in many tissues and is upregulated at sites of injury12

  • human studyIn osteoarthritis (OA), serine proteases contribute to articular cartilage destruction12

  • human studyTGase activity is increased in OA cartilage12

  • human studyRT-PCR confirmed the presence of trappin-2 mRNA in OA chondrocytes12

  • human studyFibromodulin was bound to trappin-2 in cartilage12

  • human studyElevated levels of TGase activity in OA cartilage may increase levels of this serine protease inhibitor in response to injury12

  • human studyThe expression of trappin-2/elafin has been shown to be differentially regulated in diseases associated with gut inflammation13

  • human studyNOD2 mRNA expression correlates with SKALP/elafin expression (r=0.65; P<0.01) in hidradenitis suppurativa skin18

  • human studyNOD2 signalling activation in hidradenitis suppurativa might contribute to pathogenesis via induction of antimicrobial peptides including elafin18

  • human studyElafin (E) and its precursor, trappin-2 (Tr) have been associated with mucosal resistance to HIV-1 infection20

  • human studyEx vivo incubation of trappin-2 with sputum from cystic fibrosis patients produced a proteolytic immunoreactive fragment with the same mass as native elafin25

  • human studyCleavage by sputum did not occur when preincubating sputum with polyclonal antibodies directed against tryptase25

  • animalElafin is a potent endogenous neutrophil elastase inhibitor that protects against myocardial inflammation and injury in preclinical models of ischaemic-reperfusion injury8

  • animalElafin is a potent endogenous neutrophil elastase inhibitor that protects against myocardial inflammation and injury in preclinical models of ischaemic-reperfusion injury9

  • animalNeutrophil EVs from patient plasma contain increased neutrophil elastase and human endogenous retrovirus K envelope and induce pulmonary hypertension in mice, mitigated by elafin, an elastase inhibitor17

  • animalIn vivo studies of intravaginal HSV-2 infection in Tr-transgenic mice (Etg) showed that despite similar virus replication in the genital tract, Etg mice had reduced viral load and TNF-α in the central nervous system compared to controls20

  • in vitroIn models of PAH, Elafin reverses obliterative changes in arteries of lung explants from PAH patients5

  • in vitroInterleukin 1beta (IL-1beta) stimulated elafin expression in cells derived from the endocervix, but not in those derived from the vaginal epithelium11

  • in vitroElafin and its precursor trappin-2 contribute to the physiological mucosal shield against luminal microbes13

  • in vitroTrappin-2/elafin acts as protease inhibitors13

  • in vitroTrappin-2/elafin acts as transglutaminase substrates13

  • in vitroTrappin-2/elafin acts as antimicrobial peptides13

  • in vitroTrappin-2/elafin acts as a regulator of pro-inflammatory transcription factors13

  • in vitroElafin inhibits cathepsin S and protease-activated receptor 2 activities14

  • in vitroElafin reduces collagen synthesis in intestinal fibroblasts14

  • in vitroIn unstimulated normal keratinocytes, SKALP/elafin expression significantly increases from 6 to 48 hours18

  • in vitroIn Pam2-stimulated normal keratinocytes, SKALP/elafin expression significantly increases from 6 to 48 hours18

  • in vitroIn MDP-stimulated normal keratinocytes, SKALP/elafin expression significantly increases from 6 to 48 hours18

  • in vitroIn unstimulated, Pam2-stimulated and MDP-stimulated hidradenitis suppurativa keratinocytes, SKALP/elafin expression significantly declines from 6 to 48 hours18

  • in vitroSKALP/elafin mRNA expression at 6 hours is significantly increased in hidradenitis suppurativa compared with normal keratinocytes under unstimulated and Pam2-stimulated conditions18

  • in vitroTrappin-2 expression was elevated by gene silencing of FLI1 at mRNA and protein levels in cultured endothelial cells19

  • in vitroFli1 occupied the PI3 promoter19

  • in vitroE is ∼130 times more potent than Tr against HIV-120

  • in vitroTr/E inhibited HIV-1 attachment and transcytosis across human genital epithelial cells (ECs)20

  • in vitroPretreatment of endometrial (HEC-1A) and endocervical (End1/E6E7) ECs with human Tr-expressing adenovirus (Ad/Tr) or recombinant Tr/E proteins before or after HSV-2 infection resulted in significantly reduced virus titers compared to controls20

  • in vitroE was ∼7 times more potent against HSV-2 infection than Tr20

  • in vitroKnockdown of endogenous Tr/E by small interfering RNA (siRNA) significantly increased HSV-2 replication in genital ECs20

  • in vitroRecombinant Tr and E reduced viral attachment to genital ECs by acting indirectly on cells20

  • in vitroLower viral replication was associated with reduced secretion of proinflammatory interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α) and decreased NF-κB nuclear translocation20

  • in vitroProtected Ad/Tr-treated ECs demonstrated enhanced interferon regulatory factor 3 (IRF3) nuclear translocation and increased antiviral IFN-β in response to HSV-220

  • in vitroTrappin-2/Elafin is a potent serine protease inhibitor which prevents excessive damage under inflammatory status21

  • in vitroTrappin-2/Elafin is locally expressed by epithelial cells and immune cells such as macrophages and γδ T cells21

  • in vitroTrappin-2/Elafin modulates the NFκB pathway21

  • in vitroTrappin-2/Elafin modulates cytokine secretion21

  • in vitroTrappin-2/Elafin modulates cell recruitment21

  • in vitroTrappin-2/Elafin possesses anti-microbial properties against viruses, fungi and bacteria21

  • in vitroHuman lungs contain secretory leukocyte protease inhibitor (SLPI), elafin and its biologically active precursor trappin-2 (pre-elafin)22

  • in vitroElafin and trappin-2 are low-molecular weight inhibitors involved in controlling proteolytic activities of neutrophil serine proteases including elastase, proteinase 3 and cathepsin G22

  • in vitroTrappin-2 and to a lesser extent, elafin can be linked covalently to various extracellular matrix proteins by tissue transglutaminases and remain potent protease inhibitors22

  • in vitroSLPI is composed of two distinct domains, each of which is about 40% identical to elafin22

  • in vitroTrappin-2 and elafin have consensus transglutaminase sequences, unlike SLPI22

  • in vitroType 2 tissue transglutaminase and plasma transglutaminase activated factor XIII can covalently bind SLPI to fibronectin or elastin22

  • in vitroCross-linked SLPI retains the ability to inhibit target proteases elastase and cathepsin G22

  • in vitroThe transglutamination substrate status of the cementoin domain of trappin-2 can be transferred from one protein to another, suggesting it may provide transglutaminase-dependent attachment properties for engineered proteins22

  • in vitroTrappin-2/Elafin is a serine protease inhibitor that plays a major role as an anti-inflammatory mediator at mucosal surfaces23

  • in vitroTrappin-2/Elafin has antibacterial activity against Gram-positive and Gram-negative bacterial and fungal pathogens23

  • in vitroPrimary uterine, Fallopian tube, cervical and ectocervical epithelial cells produce Trappin-2/Elafin constitutively23

  • in vitroProduction of Trappin-2/Elafin is enhanced following stimulation with Poly(I:C), especially by uterine cells23

  • in vitroThe mechanism of HIV-1 inhibition by Trappin-2/Elafin is likely a direct interaction between HIV-1 and Trappin-2/Elafin23

  • in vitroElafin and its precursor trappin prevent neutrophil proteinase-mediated lung tissue destruction24

  • in vitroMyeloperoxidase/H2O2 and N-chlorosuccinimide oxidation significantly lowers the affinities of elafin and trappin for neutrophil elastase (NE) and proteinase 3 (Pr3)24

  • in vitroOxidation of elafin and trappin causes an increase in the rate of inhibitory complex dissociation24

  • in vitroOxidized elafin and trappin are unable to efficiently inhibit the elastolytic activity of NE and Pr3 despite maintaining reasonable affinities24

  • in vitroAt physiological concentration, fully oxidized elafin does not inhibit more than 30% of an equimolar concentration of NE or Pr324

  • in vitroSerine and cysteine proteases preferentially cleaved trappin-2 within its non-inhibitory N-terminal moiety25

  • in vitroCathepsin L, cathepsin K, plasmin, trypsin and tryptase were able to release elafin by cleaving the Lys 38-Ala 39 peptide bond in trappin-225

  • in vitroPurified tryptase appeared to be efficient at releasing elafin25

  • in vitroIncubation of trappin-2 with purified mast cells challenged with anti-immunoglobulin E or calcium ionophore A23187 resulted in rapid generation of elafin25

  • in vitroProteolytic release of elafin from trappin-2 was inhibited in the presence of a tryptase inhibitor, suggesting mast cell tryptase was involved25

  • in vitroTryptase could likely be involved in the maturation of trappin-2 into elafin under physiological conditions25

  • in vitroLow-molecular-mass neutrophil elastase inhibitors have been shown to be important in the control of lung inflammation26

  • in vitroSecretory leucocyte proteinase inhibitor (SLPI) and elastase-specific inhibitor/SKALP (skin-derived antileucoproteinase)/elafin have been shown to have 'defensin'-like antimicrobial activities26

  • in vitroThese inhibitors have antimicrobial properties in vitro against bacteria, fungi and, potentially, HIV26

  • in vitroLipopolysaccharide is able to up-regulate SLPI production in macrophages in vitro26

  • in vitroRecombinant SLPI added to human monocytes or transfection of macrophages with SLPI can down-regulate pro-inflammatory mediators such as tumour necrosis factor26

  • expert opinionElafin inhibits elastase, an enzyme that is increased in pulmonary hypertension and is a major factor in the development of PAH3

  • expert opinionElafin is an endogenous human protein composed of an N-terminal transglutaminase substrate motif and a C-terminal WAP (whey acidic protein)-domain with antiproteolytic properties4

  • expert opinionElafin is expressed predominantly in epithelial tissue4

  • expert opinionElafin potently inhibits the neutrophil-derived serine proteases elastase and proteinase-3 by a competitive tight-binding mechanism4

  • expert opinionElafin inhibits EVE (endogenous vascular elastase)4

  • expert opinionElafin is identical to the human protein elafin with high specificity for tissue destroying and inflammation promoting proteases5

  • expert opinionElafin is an epithelial host-defense protein that is absent in normal skin but highly expressed in inflamed skin keratinocytes6

  • expert opinionElafin and its precursor trappin-2 are known for their contribution to the physiological mucosal shield against luminal microbes13

  • expert opinionThe protective effects of trappin-2/elafin in the gut are mediated through pleiotropic modes of action: acting as protease inhibitors, transglutaminase substrates, antimicrobial peptides or as a regulator of pro-inflammatory transcription factors13

  • expert opinionElafin is a human protein that is produced naturally in the skin, lung and breast15

  • expert opinionElafin protects tissue from destruction by the immune system15

  • expert opinionElafin blocks the activity of destructive enzymes that are involved in inflammatory reactions15

  • expert opinionPeptides interact with specific receptors to elicit highly selective biological responses, analogous to those induced by larger biologics, yet with enhanced pharmacokinetic flexibility16

  • expert opinionPeptides often demonstrate higher specific activity per unit mass, i.e., ~15-60 times that of antibodies, due to their lower molecular weight and more efficient receptor engagement16

  • expert opinionElafin is an elastase inhibitor17

  • expert opinionPeptides are molecules composed of up to 40 to 50 amino acids27

  • expert opinionPeptides occupy a distinct biochemical and regulatory niche between small-molecule drugs (generally <500 Daltons) and large biological proteins (>5000 Daltons)27

  • expert opinionPeptides function as potent signaling molecules for numerous physiological processes27

  • theoreticalElafin is a biological/biotechnological origin active substance1

  • theoreticalElafin is a potent endogenous neutrophil elastase inhibitor that protects against myocardial inflammation and injury in preclinical models of ischaemic-reperfusion injury7

  • theoreticalThe contribution of trappin-2/elafin to mucosal protection is particularly relevant in the gut due to constant microbial exposure13

  • theoreticalTrappin-2/pre-elafin is an endogenous inhibitor of human neutrophil elastase involved in inflammation, innate immunity and vascular remodelling19

  • theoreticalOxidized elafin has reasonable affinity for NE and Pr3 theoretically sufficient to form tight binding complexes in lung secretions24

Dosing

Based on 5 human trial findings and 2 theoretical findings.

  • human trialElafin was administered as an infusion in a randomised-controlled trial2

  • human trialElafin will be administered subcutaneously daily for 7 days in normal healthy subjects followed over a 28 day time period3

  • human trial87 patients undergoing CABG surgery were randomised 1:1 to intravenous elafin 200 mg or saline placebo administered after induction of anaesthesia and prior to sternotomy7

  • human trialElafin 200 mg was administered intravenously after induction of anaesthesia and prior to sternotomy8

  • human trial87 patients undergoing CABG surgery were randomised 1:1 to intravenous elafin 200 mg or saline placebo administered after induction of anaesthesia and prior to sternotomy9

  • theoreticalElafin is formulated as a solution for infusion1

  • theoreticalElafin is administered intravenously1

How the body handles it

Based on 5 human trial findings and 1 theoretical finding.

  • human trialPharmacokinetic/pharmacodynamic (PK/PD) and immunogenicity parameters in blood sample will be assessed including AUC0-last3

  • human trialElafin infusion was safe and resulted in >3000-fold increase in plasma elafin concentrations7

  • human trialElafin resulted in >3000-fold increase in plasma elafin concentrations8

  • human trialElafin resulted in >3000-fold increase in plasma elafin concentrations9

  • human trialElafin achieved >50% inhibition of elastase activity in the first 24 h9

  • theoreticalElafin has a short half-life14

Safety and side effects

Based on 6 human trial findings, 5 expert opinion findings and 1 theoretical finding.

  • human trialSafety and tolerability will be determined on the basis of adverse events reported and the severity of adverse events3

  • human trialIn a Phase I clinical trial, elafin was well tolerated4

  • human trialNo safety concerns after treatment of 75 patients in three randomized, double-blind, placebo-controlled clinical trials5

  • human trialElafin infusion was safe8

  • human trialElafin infusion was safe9

  • human trialThe excellent tolerability of Elafin in human subjects was demonstrated in a Phase I clinical single dose escalating study15

  • expert opinionPeptides generally demonstrate favorable safety profiles with minimal adverse events, effective target engagement, and clinically meaningful efficacy16

  • expert opinionA parallel and pervasive gray market has emerged, driven by direct-to-consumer sales of unapproved peptides27

Show 4 more findings

  • expert opinionUnapproved peptides are frequently carrying disclaimers like 'research chemical' or 'not for human consumption' to circumvent regulatory oversight27

  • expert opinionUnapproved peptides are aggressively marketed to the general public through social media and online forums27

  • expert opinionPeptides produced on the gray market are not subject to Good Manufacturing Practice (cGMP) guidelines or regulatory oversight27

  • theoreticalElafin did not have marketing authorization at the time of this trial1

What people use it for

Based on 2 human trial findings, 10 expert opinion findings and 3 theoretical findings.

  • human trialPerioperative elafin administration reduces post-ischaemic inflammatory myocardial injury following coronary artery bypass graft surgery2

  • human trialElafin is being developed for treatment of PAH3

  • expert opinionPhase II trials are underway to investigate the therapeutic effects of elafin on post-operative inflammation and the clinical consequences of major surgery4

  • expert opinionPhase II trials focus on reduction of post-operative morbidity after oesophagus cancer surgery, coronary artery bypass surgery and kidney transplantation4

  • expert opinionElafin has received orphan drug designations in the USA and EU for PAH treatment5

  • expert opinionTrappin-2/elafin contribution seems to be particularly relevant in the gut, where the exposure of host tissues to heavy loads of microbes is constant and contributes to mucosa-associated pathologies13

  • expert opinionTherapeutic potential of trappin-2/elafin delivery at the intestinal mucosa surface is being considered13

  • expert opinionTrappin-2/elafin mucosal delivery should be considered to ensure intestinal tissue repair13

Show 7 more findings

  • expert opinionElafin is a highly promising active compound for the treatment of inflammatory lung diseases15

  • expert opinionElafin is a highly promising active compound for the treatment of severe reperfusion injuries occurring after heart attacks, serious injuries and organ transplantation15

  • expert opinionElafin is investigated for use/treatment in inflammatory disorders15

  • expert opinionTrappin-2/Elafin might be an important endogenous microbicide of the female reproductive tract that is protective against HIV-123

  • theoreticalTherapeutic potential of trappin-2/elafin delivery at the intestinal mucosa surface is being considered13

  • theoreticalTrappin-2/elafin mucosal delivery may ensure intestinal tissue repair13

  • theoreticalIn vivo oxidation of elafin strongly impairs its activity in inflammatory lung diseases24

Other findings

Based on 2 expert opinion findings and 1 theoretical finding.

  • expert opinionChallenges remain in improving peptide stability and delivery, with innovations in cyclization, conjugation, and nano-formulation showing promise16

  • expert opinionGlobal sales of approved peptide drugs will likely reach $75 billion USD by 202827

  • theoreticalElafin was not designated as an orphan drug1

Points of contention

Where the evidence is unsettled, thin, or says less than the popular claim — worth knowing before you draw conclusions.

Contested

Elafin's key CABG trial missed its primary endpoint despite strong biomarker effects

The 87-patient randomised CABG trial showed elafin produced a >3000-fold rise in plasma elafin and >50% elastase inhibition, yet did not reduce myocardial injury over 48 h (AUC troponin I ratio 0.74, p=0.18) and had no effect on infarction or inflammation markers; only a post hoc analysis showed lower 6-hour troponin I (p=0.035). Company (Tiakis) material meanwhile describes CABG treatment as producing 'postoperative reduction of troponin I,' a more favourable framing than the trial's own null primary result.

Single source

The ~4–8 hour half-life figure comes only from a tier-3 vendor page

The specific half-life estimate of ~4–8 hours is reported only by a tier-3 vendor/research web profile; other sources describe elafin merely as having 'a short half-life' without quantification.

Single source

The 75-patient safety claim across three trials comes only from the developer

The statement of no safety concerns after treating 75 patients in three randomized, double-blind, placebo-controlled trials, and the PAH orphan drug designations, are reported by the company Tiakis Biosciences rather than an independent source.

Other

Elafin is not approved for human therapeutic use

Sources indicate elafin remains investigational (Phase I/II), had no marketing authorization at trial time and is not designated as an orphan drug in one EU registration, and a vendor profile explicitly states it is not approved for human therapeutic use.

Preprint

General peptide market and safety context comes from a preprint

Broad claims about peptide definitions, the projected $75 billion market by 2028, and gray-market safety concerns come from a tier-3 preprint review not specific to elafin.

Using it with other compounds

Check a stack
  • TeduglutideComplementary

    May be complementary

    Teduglutide drives intestinal epithelial growth and barrier repair through the GLP-2 receptor, while elafin protects that same mucosa by neutralizing destructive proteases and calming inflammation. Different mechanisms both supporting gut mucosal integrity and repair.

    Tier 3Largely anecdotal — commonly discussed

    Shares mucosal repair · tissue repair

  • LL-37Complementary

    May be complementary

    Both are human host-defense molecules but hit different targets: LL-37 is a cathelicidin that directly punctures microbial membranes, while elafin blocks the destructive enzymes (elastase, proteinase 3) that neutrophils release. Together they cover both direct killing and protection of the tissue from friendly-fire enzyme damage, converging on mucosal defense and repair.

    Tier 3Largely anecdotal — commonly discussed

    Shares innate immune · antimicrobial · anti inflammatory · tissue repair

  • LactoferrinComplementary

    May be complementary

    Lactoferrin defends by sequestering iron away from microbes and calming inflammation, while elafin blocks neutrophil serine proteases. They are two arms of innate mucosal immunity working through different mechanisms toward the same goal of infection control and reduced inflammatory tissue damage.

    Tier 3Largely anecdotal — commonly discussed

    Shares innate immune · antimicrobial · anti inflammatory

  • KPVComplementary

    May be complementary

    Both dampen inflammation at mucosal surfaces largely by restraining NF-κB signaling, but by different means: KPV (an α-MSH fragment) suppresses inflammatory cytokines and stabilizes IκBα, while elafin blocks tissue-destroying proteases. In a gut/mucosal setting they address inflammation and barrier protection from complementary angles.

    Tier 3Largely anecdotal — commonly discussed

    Shares innate immune · anti inflammatory · NF kB modulation

  • TB-500Complementary

    May be complementary

    TB-500 promotes cell migration, angiogenesis and matrix remodeling for wound healing, while elafin protects healing tissue by inhibiting neutrophil proteases and suppressing NF-κB inflammation. Distinct mechanisms both favoring tissue repair.

    Tier 3Largely anecdotal — commonly discussed

    Shares tissue repair · anti inflammatory · NF kB modulation

  • ThymulinComplementary

    No documented conflict

    Thymulin normalizes T-cell balance and tamps down excess pro-inflammatory cytokines via NF-κB inhibition, while elafin controls neutrophil protease-driven tissue damage. They modulate adaptive and innate immunity from different angles toward a calmer, better-regulated immune response.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · NF kB modulation

  • ImunofanComplementary

    No documented conflict

    Imunofan is a thymopoietin-based immunomodulator that boosts phagocytic/antimicrobial defenses and supports tissue repair, complementing elafin's antiprotease and antimicrobial actions. Different mechanisms supporting immune balance and mucosal repair.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · tissue repair

  • PidotimodComplementary

    No documented conflict

    Pidotimod stimulates dendritic cell maturation and T-cell responses against recurrent infections, while elafin provides direct antiprotease and antimicrobial protection at epithelial surfaces. Complementary adaptive-plus-innate host defense.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · antimicrobial

  • VilonComplementary

    No documented conflict

    Vilon is an immunomodulatory bioregulator that suppresses inflammatory cytokines and normalizes immune ratios, overlapping with elafin's anti-inflammatory NF-κB modulation but acting through different (gene-regulatory) mechanisms.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · NF kB modulation

  • KlothoComplementary

    No documented conflict

    Both suppress NF-κB-driven inflammation and have antifibrotic/vascular-protective roles; Klotho works through FGF23/Nrf2/NLRP3 pathways while elafin works by inhibiting proteases and modulating vascular remodeling. Different upstream mechanisms with overlapping anti-inflammatory, antifibrotic output.

    Tier 4Theoretical — not established

    Shares anti inflammatory · NF kB modulation

  • Palmitoyl Tripeptide-1Complementary

    May be complementary

    In a skin-matrix context these are complementary: palmitoyl tripeptide-1 (Pal-GHK) stimulates collagen/elastin synthesis and suppresses MMPs, while elafin protects the dermal matrix by inhibiting elastase and other proteases that degrade elastin. One builds the matrix, the other guards it from enzymatic breakdown.

    Tier 4Theoretical — not established

    Shares anti inflammatory · dermal matrix · tissue repair

  • MatrixylComplementary

    May be complementary

    Matrixyl stimulates collagen and ECM production while inhibiting matrix-degrading proteases; elafin adds antiprotease protection of elastin/collagen by blocking neutrophil elastase. Complementary matrix-building plus matrix-protecting actions in skin repair.

    Tier 4Theoretical — not established

    Shares dermal matrix · tissue repair

  • Palmitoyl Tetrapeptide-7Complementary

    No documented conflict

    Both protect the extracellular matrix and dampen inflammation, but by non-overlapping mechanisms — Elafin blocks destructive serine proteases (elastase, proteinase 3) and modulates NF-κB, whereas Palmitoyl Tetrapeptide-7 suppresses IL-6/IL-1β and inhibits MMP-1-driven collagen breakdown. Together they cover a broader range of matrix-degrading enzymes and inflammatory drivers.

    Tier 4Theoretical — not established

    Shares dermal matrix · anti inflammatory

  • GLOWComplementary

    No documented conflict

    Elafin protects tissue by inhibiting destructive neutrophil elastase and proteinase-3 and by dampening NF-κB inflammation — a protease-inhibition mechanism distinct from GLOW's matrix-building action. By preserving elastin and the dermal matrix from enzymatic breakdown while GLOW rebuilds it, the two work on repair from opposite ends (protection vs synthesis).

    Tier 4Theoretical — not established

    Shares anti inflammatory · mucosal repair · dermal matrix · NF kB modulation · tissue repair

  • Larazotide AcetateComplementary

    No documented conflict

    Both peptides are reported to act on protease-activated receptor-2 (PAR-2) and to protect mucosal surfaces: elafin inhibits destructive neutrophil proteases and PAR-2 signaling while larazotide restores tight junctions. Their overlapping mucosal-protective and anti-inflammatory actions via partly different targets make them a complementary gut/mucosal pairing.

    Tier 4Theoretical — not established

    Shares mucosal repair · anti inflammatory · tissue repair

  • ThymalinComplementary

    No documented conflict

    Elafin is an innate-immune protease inhibitor that protects tissue and quiets NF-kB-driven inflammation at mucosal surfaces, a distinct mechanism from Thymalin's thymic adaptive-immune restoration. Both converge on lowering NF-kB inflammatory tone through different upstream biology, so they are complementary rather than redundant.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · NF kB modulation

  • Thymosin Alpha-1Complementary

    No documented conflict

    Elafin is an innate-defense protein that blocks destructive neutrophil proteases and has direct antimicrobial and antiviral activity, especially at mucosal surfaces. Thymosin Alpha-1 instead modulates T-cells, NK cells and cytokine tone. Different mechanisms converging on antimicrobial defense and inflammation control make them complementary rather than overlapping.

    Tier 4Theoretical — not established

    Shares innate immune · anti inflammatory · antimicrobial

  • Alpha-MSHComplementary

    Worth caution

    Elafin protects tissue by inhibiting neutrophil serine proteases and dampening NF-κB, whereas alpha-MSH suppresses inflammation through melanocortin/cAMP signaling and NF-κB. Both also carry antimicrobial activity. These are different upstream mechanisms landing on the same goal of resolving inflammation and protecting mucosal/tissue surfaces, making them a complementary pairing.

    Tier 4Theoretical — not established

    Shares anti inflammatory · antimicrobial · NF kB modulation

Safety and side effects

Safety and Tolerability

Elafin is not approved for human therapeutic use and remains investigational.

  • DrugBank reports that excellent tolerability of elafin in human subjects was demonstrated in a Phase I single-dose escalating study, and lists 1 Phase 1 trial with no Phase 0, 2, 3 or 4 trials.
  • In the 87-patient CABG trial, intravenous elafin 200 mg infusion was reported to be safe.
  • The developer Tiakis reports no safety concerns after treatment of 75 patients in three randomized, double-blind, placebo-controlled clinical trials. This combined safety statement, and the PAH orphan drug designations, are reported by the company rather than an independent source.
  • The Phase I trial (NCT03522935) was designed to assess safety and tolerability via adverse events and their severity, along with pharmacokinetic/pharmacodynamic and immunogenicity parameters — indicating immunogenicity is a monitored consideration for this protein therapeutic.

General peptide context

A review16 states that peptides generally demonstrate favorable safety profiles with minimal adverse events and interact with specific receptors for highly selective responses, while noting challenges in stability and delivery. A tier-3 preprint review separately warns of a pervasive gray market of unapproved peptides sold direct-to-consumer with 'research chemical' disclaimers, marketed via social media and not subject to cGMP guidelines or regulatory oversight.

Efficacy caveats relevant to safety framing

The pivotal CABG trial missed its primary endpoint despite strong biomarker effects, and most other disease-specific findings come from in vitro, animal or observational studies. An oxidation study24 further notes that oxidation by myeloperoxidase/H2O2 significantly impairs elafin's ability to inhibit elastase and proteinase 3 in inflammatory settings, which may limit its activity in inflammatory lung disease.

Reconstitution and handling

Dosing

No dose has been established for this compound. Elafin is not approved for human therapeutic use and no regulatory label exists for it, so the figures below are what research sources report — not guidance.

  • The Phase I trial (NCT03522935) planned subcutaneous administration daily for 7 days in healthy subjects, followed over 28 days, at doses of 0.03, 0.06, 0.10, 0.15 and 0.18 mg/kg across 5 groups of 6 subjects each.
  • The 87-patient CABG trial used a single intravenous dose of elafin 200 mg (formulated as a 200 mg concentration solution for IV infusion), administered after induction of anaesthesia and prior to sternotomy. In that trial this produced a >3000-fold increase in plasma elafin and >50% elastase inhibition in the first 24 hours — yet did not reduce myocardial injury over 48 hours.
  • A vendor profile reports that in research settings elafin is typically administered via topical and intravenous routes(vendor claim).

No human trial has established an efficacious dose for any indication.

Pharmacokinetics

  • A vendor profile (tier-3, single source) reports a half-life of approximately 4–8 hours(vendor claim). Other sources describe elafin only as having 'a short half-life'14 without quantification.
  • The Phase I trial planned to measure pharmacokinetic/pharmacodynamic and immunogenicity parameters including AUC0-last in blood.

Preparation notes

Elafin is a recombinant protein/peptide biological (CAS 820211-82-3; reported ~10 kDa mass26) that has been formulated as a solution for intravenous infusion in trial settings and delivered subcutaneously in the Phase I protocol. As with other protein therapeutics, immunogenicity is a monitored parameter. Reconstitution and handling specifics for any research material should follow the supplier's documentation; no standardized preparation protocol is established for unapproved use.

Sources

Ordered by evidence quality — the strongest first.

  1. Clinical Trials Register(opens in a new tab)
    Tier 1Web · clinicaltrialsregister.eu
  2. EudraCT Number 2010-019527-58 - Clinical trial results - EU Clinical Trials Register(opens in a new tab)
    Tier 1Web · clinicaltrialsregister.eu
  3. NCT03522935 | Subcutaneous Elafin in Healthy Subjects(opens in a new tab)
    Tier 1Web · clinicaltrials.gov
  4. Therapeutic potential of human elafin - PubMed(opens in a new tab)
    Tier 1Web · pubmed.ncbi.nlm.nih.gov
  5. tiakis (formerly Proteo Biotech AG) Elafin Enters the Clinic For Subcutaneous Use In Pulmonary Arterial Hypertension - Tiakis Biotech(opens in a new tab)
    Tier 1Web · tiakis.bio
  6. Elafin level in lichen planus.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov · 2024
  7. Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial - Glasgow Caledonian University(opens in a new tab)
    Tier 1Web · researchonline.gcu.ac.uk · 2015
  8. Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial(opens in a new tab)
    Tier 1Web · doi.org · 2015
  9. Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial - University of Edinburgh Research Explorer(opens in a new tab)
    Tier 1Web · research.ed.ac.uk · 2015
  10. Secretory leukocyte protease inhibitor and elafin/trappin-2: versatile mucosal antimicrobials and regulators of immunity.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov · 2010
  11. Elafin (SKALP/Trappin-2/proteinase inhibitor-3) is produced by the cervix in pregnancy and cervicovaginal levels are diminished in bacterial vaginosis.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov · 2009
  12. The serine protease inhibitor trappin-2 is present in cartilage and synovial fluid in osteoarthritis.(opens in a new tab)
    Tier 1PubMed · pubmed.ncbi.nlm.nih.gov · 2006
  13. Elafin and its precursor trappin‐2: What is their therapeutic potential for intestinal diseases?(opens in a new tab)
    Tier 2Web · pmc.ncbi.nlm.nih.gov
  14. Elafin Reverses Intestinal Fibrosis by Inhibiting Cathepsin S-Mediated ...(opens in a new tab)
    Tier 2Web · cmghjournal.org
  15. Elafin: Uses, Interactions, Mechanism of Action(opens in a new tab)
    Tier 2Web · go.drugbank.com
  16. Safety and Efficacy of Peptide-Based Therapeutics in Health Sciences(opens in a new tab)
    Tier 2Web · biomedgrid.com
  17. Endogenous Retroviral Elements Generate Pathologic Neutrophils in Pulmonary Arterial Hypertension.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2022
  18. NOD2 signalling in hidradenitis suppurativa.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2021
  19. A potential contribution of trappin-2 to the development of vasculopathy in systemic sclerosis.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2019
  20. Antiviral activity of trappin-2 and elafin in vitro and in vivo against genital herpes.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2013
  21. The WAP protein Trappin-2/Elafin: a handyman in the regulation of inflammatory and immune responses.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2012
  22. Secretory leukocyte protease inhibitor (SLPI) is, like its homologue trappin-2 (pre-elafin), a transglutaminase substrate.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2011
  23. Trappin-2/Elafin: a novel innate anti-human immunodeficiency virus-1 molecule of the human female reproductive tract.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2010
  24. Oxidized elafin and trappin poorly inhibit the elastolytic activity of neutrophil elastase and proteinase 3.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2005
  25. Proteolytic susceptibility of the serine protease inhibitor trappin-2 (pre-elafin): evidence for tryptase-mediated generation of elafin.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2005
  26. Antimicrobial activity of antiproteinases.(opens in a new tab)
    Tier 2PubMed · pubmed.ncbi.nlm.nih.gov · 2002
  27. Safety and Efficacy of Approved and Unapproved Peptide Therapies for ...(opens in a new tab)
    Tier 3Web · preprints.org

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