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collagenase (Plaquase / Nucleolysin / lipolysin)

✓ Approved

Johnson & Johnson Services, Inc. · 治疗药物

什么是 collagenase？

collagenase 是一种治疗药物，由Johnson & Johnson Services, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Topical。

药物档案

商品名Plaquase, Nucleolysin, lipolysin
公司Johnson & Johnson Services, Inc.
给药途径Injectable (Others), Topical
状态Approved
来源： ClinicalTrials.gov, Johnson & Johnson Services, Inc.

治疗适应症

collagenase 针对 10 个适应症，涉及 7 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersDecubitus ulcer✓ Approved
Injury, poisoning and procedural complicationsThermal burn✓ Approved
Skin and subcutaneous tissue disordersDiabetic foot✓ Approved
Musculoskeletal and connective tissue disordersDupuytren's contracture✓ Approved
Eye disordersGlaucoma✓ Approved

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相关研究文献

PubMedFree radical biology & medicine2026-08-04

CKLF1 Upregulation Exacerbates Secondary Brain Injury after Intracerebral Hemorrhage by Promoting Neuronal Ferroptosis and Oxidative Stress.

Yang Shangwen S, Liu Yupei Y, Zhang Xinyi X, Jiang Hongxiang H et al.

Secondary brain injury (SBI) following spontaneous intracerebral hemorrhage (ICH) is a critical determinant of neurological outcome. It is closely associated with neuronal death, and inflammatory responses. However, current research on SBI after ICH remains limited, and effective therapeutic targets are still lacking. In this study, a collagenase-induced intracerebral hemorrhage (ICH) model was employed, and experiments were conducted 24 h after hemorrhage induction. For in vitro experiments, differentiated PC12 cells were stimulated with hemin and the CKLF1 agonist peptide C27 to evaluate the potential of CKLF1 to induce neuronal ferroptosis. Mechanistically, the CKLF1 antagonist peptide C19, the CCR5 inhibitor Maraviroc (MVC), and a p38 MAPK inhibitor were applied, in combination with immunoprecipitation (Co-IP) assays and overexpression of p53 site mutation, to elucidate the molecular mechanisms underlying CKLF1-induced ferroptosis in PC12 cells. In vivo, the effects of CKLF1 knockdown on secondary brain injury after ICH were assessed using quantitative real-time PCR (qPCR), Western blotting (WB), immunohistochemistry (IHC), and immunofluorescence (IF) analyses. Mechanistic studies revealed that CKLF1 binds to its receptor CCR5 to activate p38 MAPK, which promotes ferroptosis by regulating p53 phosphorylation and nuclear translocation, while the mutation of p53 partially reversed the effect. This signaling cascade leads to the downregulation of ferroptosis-suppressing proteins (SLC7A11 and GPX4) and the upregulation of pro-ferroptotic proteins (COX2 and ACSL4), thereby exacerbating lipid peroxidation and oxidative stress. Conversely, AAV-mediated knockdown of CKLF1 significantly suppressed this ferroptotic signaling pathway in vivo/vitro, reduced iron deposition and neuronal ferroptosis in perihematomal tissue, improved blood-brain barrier (BBB) integrity, inhibited microglial activation, and enhanced both neurological function scores and 7-day survival rates in ICH rats. The present study identifies CKLF1 as a previously unrecognized regulator of neuronal ferroptosis following ICH through the CCR5/p38/p53 signaling pathway. These findings provide new mechanistic insights into ICH pathogenesis and highlight CKLF1 as a promising therapeutic target for precision treatment of hemorrhagic stroke.

PMID 42546807
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PubMedZhonghua shao shang yu chuang mian xiu fu za zhi2026-08-04

[Influence and mechanism of PBNP combined with mouse ADSCs on full-thickness skin defect wounds in diabetic mice].

Zhang X W XW, Xu S Y SY, Han Y J YJ, Li X M XM et al.

Objective: To investigate the influence and mechanism of Prussian blue nanoparticles (PBNPs) combined with mouse adipose-derived mesenchymal stem cells (ADSCs) on full-thickness skin defect wounds in diabetic mice. Methods: This study was an experimental study using group design and repeated-measures design. PBNPs were prepared by hydrothermal synthesis, and their morphology was characterized by transmission electron microscopy. ADSCs were isolated from five male 6-8-week-old Institute of Cancer Research (ICR) mice, USA via collagenase digestion. The cells were divided into control group cultured under routine conditions, high-glucose group cultured with glucose in a final molarity of 30.0 mmol/L, and low-PBNP group and high-PBNP group pretreated with 10 or 20 μg/mL PBNP for 12 h, respectively, followed by the same treatment as in high-glucose group. After 24 h of culture, cell viability was assessed using the cell counting kit-8, the proportion of senescent cells in the cells was detected by β-galactosidase staining, and the protein expression levels of senescence-associated proteins p16 and p21 were determined by Western blotting. Twenty-four male 6-8-week-old ICR mice were used to establish the diabetic model. A full-thickness skin defect wound was then created on the back of each mouse. The injured mice were divided into four groups (with 6 mice in each group) according to the random number table method, including control group with wounds treated with normal saline, ADSC group with wounds treated with normal saline containing 5×106 ADSC (the same number of cells used below), low-PBNP group and high-PBNP group with wounds treated with normal saline containing ADSC pretreated with 10 and 20 μg/mL PBNP for 12 h, respectively. Wound healing was observed at post-injury day (PID) 0 (immediately), 3, 7, 10, and 14. The percentage of remaining wound area was calculated at PID 3, 7, 10, and 14. At PID 7, the protein expression levels of the cell proliferation markers Ki67 and vascular endothelial growth factor (VEGF) in wound tissue were detected by immunofluorescence method. At PID 14, the expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-10 in wound tissue were determined by enzyme-linked immunosorbent assay. Results: PBNPs exhibited a dispersed regular cubic structure. After 24 h of culture, compared with those in control group, cells in high-glucose group showed a significantly lower cell viability (P<0.05), a significantly higher proportion of senescent cells (P<0.05), and significantly higher protein expression levels of p16 and p21 (P<0.05). Compared with those in high-glucose group, cells in low-PBNP and high-PBNP groups showed significantly higher cell viability (P<0.05), significantly lower proportions of senescent cells (P<0.05), and significantly lower protein expression levels of p16 and p21 (P<0.05). From PID 0 to 14, the wounds of mice in all four groups healed gradually. At PID 3, 7, 10, and 14, the percentages of remaining wound area of mice in high-PBNP group were (75.3±3.1)%, (46.7±2.5)%, (24.0±5.2)%, and (8.0±1.0)%, respectively, all significantly lower than (85.0±2.0)%, (62.7±3.1)%, (46.7±3.8)%, and (19.3±2.1)% in ADSC group (P<0.05). At PID 7, the percentage of remaining wound area of mice in ADSC group was significantly lower than that in control group ((77.3±3.2)%, P<0.05). At PID 7, the protein expression levels of Ki67 and VEGF of cells in ADSC group were significantly higher than those in control group (P<0.05), the protein expression levels of Ki67 of cells in low-PBNP and high-PBNP groups and the protein expression level of VEGF of cells in high-PBNP group were significantly higher than those in ADSC group (P<0.05). At PID 14, compared with those in control group, wound tissue in ADSC group showed a significantly higher expression level of IL-10 (P<0.05) and significantly lower expression levels of TNF-α, IL-1β, and IL-6 (P<0.05); compared with those in ADSC group, wound tissue in low-PBNP and high-PBNP groups showed significantly higher expression levels of IL-10 (P<0.05) and significantly lower expression levels of TNF-α, IL-1β, and IL-6 (P<0.05). Conclusions: PBNP can inhibit high glucose-induced senescence of mouse ADSCs. PBNP combined with mouse ADSCs is more effective than mouse ADSCs alone in promoting cell proliferation and angiogenesis in full-thickness skin defect wounds of diabetic mice, inhibiting the release of inflammatory cytokines, and accelerating wound healing.

PMID 42547440
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PubMedPloS one2026-08-03

Optimization of extracellular vesicle extraction from hepatic tissue interstitial fluid and analysis of their ncRNA expression profiles.

Liu Shubo S, Fu Yuxuan Y, Guo Hua H, Li Hailin H et al.

To address the limited tissue specificity of extracellular vesicles (EVs) derived from blood and other body fluids, this study isolated small EVs (sEVs) from the tissue interstitial fluid (TIF) of hepatocellular carcinoma (HCC) and adjacent tissues. The expression profiles of non-coding RNAs (ncRNAs) were analyzed to identify more specific diagnostic biomarkers. An optimized protocol for TIF-sEV extraction was established, which combined enzymatic digestion (Collagenase D and DNase I) with differential and ultracentrifugation. The isolated sEVs were characterized using nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM), and western blotting (WB). The expression of 33 candidate ncRNAs (11 lncRNAs from TCGA-LIHC and 22 miRNAs from TCGA-LIHC and GSE302990) in TIF-sEVs was analyzed by qRT-PCR and integrated with clinical parameters via LASSO regression. The optimal extraction conditions were determined to be digestion with Collagenase D (2 mg/mL) and DNase I (40 U/mL) for 30 minutes. The obtained EVs exhibited typical morphology, a particle size below 200 nm, and expressed canonical EV marker proteins (ALIX, CD63) as well as the hepatocyte-specific membrane protein ASGPR. qRT-PCR analysis revealed specific enrichment of six lncRNAs (e.g., AL031985, TMCC1-AS1) and eleven miRNAs (e.g., miR-1224-5p, miR-483-5p) in TIF-sEVs. LASSO regression applied to all 33 candidate ncRNAs and clinical parameters identified a combined diagnostic signature comprising ALB, PLT, DBIL, lncRNA GAS5, and miR-194-5p, which achieved an area under the curve (AUC) of 0.960. This study establishes an efficient and stable system for the isolation and characterization of TIF-sEVs from liver tissue. Furthermore, it identifies multiple non-coding RNAs (ncRNAs) that are enriched in TIF-sEVs, thereby providing potential novel diagnostic biomarkers for the differential diagnosis and prognosis evaluation of HCC.

PMID 42546027
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PubMedJournal of ethnopharmacology2026-08-01

Polyphenol-Rich Cistus salviifolius L. Extract Exerts Fungicidal Activity Against Dermatophytes Through Severe Ultrastructural Disruption.

Álvarez-Martínez Francisco Javier FJ, Denil Eléa E, Pons-Rocamora Nerea N, Fernandes Chantal C et al.

Cistus salviifolius L. (Cistaceae) has long been employed in Mediterranean traditional medicine for the topical treatment of skin disorders, including infections, wounds, and inflammatory conditions. Despite its recognized ethnobotanical relevance, its antidermatophytic potential remains insufficiently characterized. This study aimed to pharmacologically validate the traditional use of C. salviifolius against cutaneous fungal infections by evaluating the antifungal activity of a polyphenol-rich extract against dermatophytes, investigating its mechanism of action, and assessing its skin-protective properties in a reconstructed human epidermis (RHE) model. Antifungal activity was determined by broth microdilution assays following EUCAST guidelines to establish minimum inhibitory and fungicidal concentrations. Ultrastructural alterations were examined by transmission electron microscopy (TEM). The extract was further evaluated in dermatophyte-infected RHE through fungal DNA quantification, transepithelial electrical resistance measurements, histological analysis, and cytokine release assays. Antioxidant activity and inhibition of extracellular matrix-degrading enzymes were also assessed. The extract showed selective fungicidal activity against dermatophytes, with MIC values of 78 mg/L against Trichophyton rubrum and Microsporum canis. TEM revealed severe cellular damage, including extensive vacuolization, membrane detachment, and cytoplasmic disorganization. In the RHE model, topical treatment reduced fungal burden, preserved epidermal barrier integrity, and attenuated IL-1α and IL-8 release, particularly against T. rubrum. Additionally, the extract displayed strong antioxidant activity and significantly inhibited collagenase, elastase, and hyaluronidase. These findings provide pharmacological support for the traditional use of C. salviifolius in skin infections and identify this polyphenol-rich extract as a promising multifunctional candidate for topical dermatophytosis management.

PMID 42537763
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PubMedThe journal of sexual medicine2026-07-31

Collagenase nanocapsules for the treatment of Peyronie's disease. Evaluation in fibrotic plaques obtained from human patients.

Jiménez-Jiménez Carla C, Fernández-Pascual Esaú E, Angulo Javier J, Campos-Juanatey Félix F et al.

Intraplaque injection of collagenase Clostridium histolyticum (CCH) is a therapeutic approach for treating Peyronie's disease (PD) that may represent an alternative to surgery in some patients. However, the efficacy of collagenase injection is rather variable among patients. Nanocapsules (NC) provide therapeutic advantages by allowing sustained protein release and preserving enzymatic activity. The aim was to evaluate the in vitro efficacy of preparation of polymeric NC containing collagenase in reducing human PD plaque. Polymeric nanocapsules containing collagenase type I (ColNC) or blank NC were synthesized. Enzymatic activity of ColNC and free-collagenase (Col) was determined. The impact of NC, ColNC, and Col on cell viability of commercially available fibroblasts and myofibroblasts was determined. The effects of treatments on differentiation of fibroblasts obtained from plaques of PD patients into myofibroblast and differential cell viabilities were evaluated. Plaque tissues from PD patients (n = 13) were injected with phosphate-buffered saline solution, Col (0.1%), ColNC (0.1%), or equivalent amount of NC. Seven days after, the reduction in plaque tissue weight, type 1 collagen content, and the release of protein to the medium were determined. Nanocapsules exerted protective effect for collagenase by preserving its activity for 10 days versus 48 h for Col. Although fibroblasts from PD patients were unaffected, ColNC decreased the viability of myofibroblasts by 80% compared to 20% reduction obtained by Col. Single injection of ColNC into PD plaque reduced weight by 30%, compared to 10% by Col. This was related to significant reduction in collagen content in the plaque and increased protein content in the medium. Extending CCH activity and efficacy by nanoencapsulation may reduce injection repeats and improve therapeutic response to CCH injection, potentially representing a therapeutic strategy. Superiority of ColNC was demonstrated with biochemical assays, cell culture procedures, and in vitro functional evidence in plaque tissue from PD patients. Main limitation was the relatively low number of human samples due to limited human tissue availability. Encapsulation of collagenase into polymeric NC extends enzymatic activity and efficiency to degrade fibrous PD plaque. These results suggest that treatment with ColNC may represent a potential therapeutic strategy to reduce injection repeats in the management of PD but requires validation in in vivo and clinical studies.

PMID 42536455
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PubMedVeterinary radiology & ultrasound : the official journal of the American College of Veterinary Radiology and the International Veterinary Radiology Association2026-07-29

Evaluation of Microvascular Flow Imaging and Power Doppler Ultrasonography in an Equine Model of Induced Superficial Digital Flexor Tendonitis.

Garcia-Collao Miriam R MR, Ortved Kyla K, Stefanovski Darko D, Christensen Joie L JL et al.

Superficial digital flexor tendon (SDFT) injuries are common in athletic horses and are associated with prolonged healing and high reinjury rates. Conventional ultrasonography provides structural information but limited physiologic assessment. This study compared microvascular imaging (MVI) and Power Doppler (PD) for evaluating vascular changes in a collagenase-induced equine SDFT injury model and assessed the effect of scanning technique on vascular signal detection. Eight adult Thoroughbred horses underwent bilateral collagenase-induced SDFT injury, with one forelimb randomly assigned to intralesional autologous protein solution treatment and the contralateral limb receiving intralesional saline. Ultrasonographic examinations were performed at baseline and Weeks 0, 2, 4, 8, and 12 post-injury. Longitudinal and transverse MVI and PD images were evaluated using semiquantitative vascularity scores and quantitative vascularity ratios. Mixed-effects Poisson regression accounted for repeated measures and assessed effects of imaging modality, time, scanning plane, weight-bearing (WB) stance, stand-off use, and observer experience. MVI detected higher vascularity than PD at all post-injury time points (2.04 [95% confidence intervals-CI: 1.73-2.34] vs. 0.87 [0.64-1.10]) with peak vascularity at Week 2 followed by gradual decline during healing. Quantitative vascularity ratios mirrored semiquantitative findings. Longitudinal imaging yielded greater vascular detection than transverse imaging for both techniques (1.97 [95% CI: 1.72-2.22] vs. 0.92 [0.69-1.15]), whereas WB status and stand-off pad use had no statistical significant effect. Observer experience influenced vascularity scores but not temporal trends. These findings demonstrate MVI detects more intratendinous vascularity than PD during SDFT injury and healing, and support its use as a complementary tool for monitoring equine tendinopathy.

PMID 42522440
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