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collagenase (Plaquase / Nucleolysin / lipolysin)

✓ Approved

Johnson & Johnson Services, Inc. · therapeutic agent

What is collagenase?

collagenase is a therapeutic agent developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via injectable (others) or topical.

Drug Profile

Brand NamesPlaquase, Nucleolysin, lipolysin
CompanyJohnson & Johnson Services, Inc.
RouteInjectable (Others), Topical
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Therapeutic Indications

collagenase is developed for 10 unique indications across 7 therapeutic areas.

Therapeutic AreaConditionPhase
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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Related Research Articles

PubMedDental materials journal2026-05-25

Improved biostability of collagen in sound and caries-affected dentin using an integrated crosslinking-remineralization treatment.

Saleha Nisar N, Hass Viviane V, Wang Yong Y

This study investigated a combined strategy using collagen crosslinking and polymer-induced liquid precursors (PILP)-based remineralization to enhance collagen biostability and resistance to collagenase degradation in sound (SD), denatured (DD), and caries-affected dentin (CAD). Ultra-thin demineralized collagen films and acid-etched dentin beams with demineralized layers (DL) were treated with 1% cranberry-extract (CR) collagen crosslinker for 30 s, followed by PILP remineralization for 1-7 days. Biostability was assessed by collagenase-induced weight loss and hydroxyproline release; structural and remineralization changes were evaluated via electron microscopes. Both CR and PILP individually improved collagen biostability, with greater effects in SD than DD. CR crosslinking was more effective than PILP alone. Notably, the combined CR-PILP approach produced the greatest enhancement in biostability. Electron microscopes confirmed that this dual treatment preserved the DL from enzymatic digestion and dramatically accelerated mineral deposition in both SD and CAD. These findings support the potential of this synergistic strategy for improving dentin restoration durability.

PMID 42178234
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PubMedbioRxiv : the preprint server for biology2026-05-25

Neutrophil migration in the lung is altered by alveolar collapse and stretch.

Deng Yuqing Y, Kang Byungjun B, Shi Linzheng L, Min Chanhong C et al.

Heterogeneous alveolar collapse is prevalent in inflammatory lung conditions such as chronic obstructive pulmonary disease, acute respiratory distress syndrome, and pneumonia. Although neutrophil-released proteases contribute to the tissue remodeling that leads to alveolar collapse, how this altered mechanical environment in turn affects neutrophil migration remains largely unexplored. In this study, we investigate how alveolar collapse and stretch influence neutrophil migration and identify the mechanical and biochemical factors that govern regional migration differences. We developed a novel precision-cut lung slice platform that generates collapsed vs non-collapsed regions within the same slice. Neutrophils in both regions were longitudinally imaged for up to 5 hours to quantify motility behavior. Migration mechanisms were probed using migration-related inhibitors, collagenase, and cigarette smoke extract. A crystal ribcage system, which preserves intact alveolar shape and the air-liquid interface, was also used to assess the effects of ventilation on neutrophil migration. Neutrophil migration was faster in the collapsed region compared to not-collapsed regions. This regional difference was eliminated by Rho-associated protein kinase (ROCK) inhibition, which selectively increased migration speed in the non-collapsed region. The regional difference persisted with the addition of collagenase and cigarette smoke extract, both of which significantly increased the migration speed in both regions. In the crystal ribcage, the preserved air-liquid interface and ventilation together enhanced neutrophil migration compared with a collapsed lung. Alveolar collapse and stretch facilitate neutrophil migration, indicating the role of localized tissue remodeling in driving neutrophil activity and further disease progression.

PMID 42182363
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PubMedComputational and structural biotechnology journal2026-05-25

Rapid 3D Immunolabeling and Light Sheet Microscopy for Quantitative Analysis of Intact Tissues.

Chen Junyu J, Ding Zhangfan Z, Biswas Lincoln L, De Angelis Jessica J et al.

Whole-organ 3-dimensional (3D) imaging of intact tissues provides high-resolution cellular and molecular insights into tissue and tumor microenvironments. However, immunolabeling and tissue clearing methods remain complex and time-consuming and often rely on toxic reagents and prolonged processing times. Here, we introduce a rapid 3D immunolabeling and light sheet microscopy platform for quantitative analysis of intact murine organs and human tissues within 2 to 2.5 d. This streamlined workflow integrates antigen retrieval, permeabilization, collagenase-based digestion, immunolabeling, dehydration, and tissue clearing into a single optimized pipeline for fast and reproducible processing of intact tissues. Notably, this ultrafast 3D imaging method is optimized for exogenous fluorescence labeling, overcoming limitations associated with endogenous fluorescence in conventional tissue clearing approaches. It enables robust quantitative analysis and detection of rare cell populations, including round α-smooth muscle actin (α-SMA)-positive cells in the thymus, while preserving overall tissue integrity and maintaining compatibility with downstream histology. Using this rapid whole-tissue imaging platform, we mapped lymphatic vessel networks across multiple organs and age groups, revealing age-associated expansion in specific endocrine tissues but not in other organs. Overall, this method provides a rapid, reproducible, and versatile approach for whole-organ and intact tissue imaging, enabling comprehensive mapping of complex tissue architectures and rare cells, and advancing quantitative light sheet-based tissue analysis and disease research.

PMID 42179916
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PubMedACS omega2026-05-25

Islet Proteome Remodeling and Proteostasis Disruption in HFSC-Fed Mice.

Gangadhara Vijayalakshmi V, Karthik Yalpi Y, Manisekaran Ravichandran R, Abraham Asha A

Chronic overnutrition promotes metabolic syndrome and imposes substantial stress on pancreatic tissue, yet the early molecular alterations within pancreatic islets remain incompletely understood. High-fat, simple-carbohydrate (HFSC) diets have previously been shown to induce pancreatic steatosis, acinar atrophy, and islet hypertrophy in C57BL/6J mice. To investigate molecular responses underlying HFSC-induced pancreatic remodeling, we analyzed proteomic alterations in collagenase-isolated pancreatic islets from male C57BL/6J mice fed a laboratory-formulated HFSC diet for 150 days (n = 3 per group). Islet proteins were profiled using label-free ESI-nanoLC-MS/MS, resulting in the identification of 386 proteins. After applying peptide-based filtering criteria (≥2 peptides, ≥1 unique peptide) and statistical thresholds (fold change ≥ 1.5 and false discovery rate (FDR)-adjusted q-value ≤ 0.05), 30 proteins were identified as differentially expressed, including 19 upregulated and 11 downregulated proteins in HFSC islets compared with controls. Functional enrichment analysis revealed significant upregulation of pathways related to cytoplasmic translation, ribosomal biogenesis, and endoplasmic reticulum (ER) protein-folding processes, indicating increased biosynthetic activity and activation of proteostasis mechanisms. In contrast, downregulated proteins were enriched in carbohydrate and lipid metabolic pathways, suggesting metabolic remodeling within pancreatic islets. Notably, stress-responsive proteins, including MANF, HYOU1, SDF2L1, and HSP90B1, were downregulated, supporting the presence of ER stress-associated proteostasis alterations under HFSC-dietary conditions. Together, these findings provide proteomic evidence of molecular adaptations associated with metabolic stress in pancreatic islets, highlighting potential pathways involved in early islet dysfunction during diet-induced metabolic syndrome.

PMID 42179566
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PubMedCell biology international2026-05-24

Establishment and Molecular Characterization of a Short-Term Primary Culture Derived From Invasive Micropapillary Carcinoma of the Breast.

Gurav Mamta M, Shetty Omshree O, Joshi Shalaka S, Gulia Seema S et al.

Invasive micropapillary carcinoma (IMPC) of the breast, a rare and aggressive subtype, represents a unique morphology of reversed polarity with higher metastatic propensity. Due to the limited availability of experimental models, understanding distinct molecular pathways and potential therapeutic targets remains challenging. This study aimed to establish patient-derived cell cultures (PDCs) from IMPC to generate viable models for in-vitro studies. Tissue samples from five IMPC cases were enzymatically disaggregated using five different cell disaggregation protocols. These cells were characterized using immunofluorescence, short tandem repeats profiling, and real-time assays for tumor marker expression profiles. RNA sequencing was performed and compared with invasive ductal carcinoma, no special type (IDC-NST), to study differential gene expression and cell polarity markers. Two short-term PDCs were successfully established from IMPC samples with an optimized collagenase-based protocol. These cultures showed an immunohistochemical profile consistent with the original tumor tissues and maintained hormone receptor and MUC1 expression status. RNA sequencing of PDCs revealed similar gene expression patterns with matched tumor tissue and revealed upregulated RAP1, MAPK, and PI3K-AKT pathways, when compared with ER/PR-matched IDC. These PDCs also showed different gene expression patterns in cell-polarity associated genes, such as cadherins CDH2, tight junction gene MARVELD2, PAR complex gene PARD6B, and downregulation of the cell polarity CRB2 gene. This study indicated the need for an optimization of cell culture conditions and the feasibility of establishing patient-derived cell cultures from IMPC. These models provide a great tool to study molecular insights, cell polarity, and therapeutic research in a rare breast cancer subtype.

PMID 42175825
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PubMedScientific reports2026-05-22

Comparative in vitro and in vivo assessment of three experimental extracellular matrix meshes for soft tissue remodeling.

Ruan Wenting W, Wang Guowei G, Qu Qiujin Q, Gai Xiaoxiao X et al.

The development of standardized cross-species evaluation frameworks is urgently needed for absorbable extracellular matrix (ECM) meshes, due to significant variations in safety and efficacy across tissue sources. This study establishes a multi-dimensional assessment system to quantify material-specific bio-functional correlations. Three ECM meshes-human acellular dermis (HAD), porcine acellular dermis (PAD), and porcine small intestinal submucosa (SIS)-were systematically characterized using integrated in vitro and in vivo analyses. Assessments included physicochemical properties (e.g., degradation kinetics via collagenase digestion), immunogenic residues (α-Gal epitopes and DNA quantification), and biocompatibility. In vivo performance was evaluated using rabbit subcutaneous (for degradation and immune response) and rat abdominal defect models (for macrophage polarization: CD206⁺/CD86⁺ ratio and collagen deposition). HAD exhibited superior structural stability (82.3% ± 1.2% residual mass after 7-day collagenase digestion), whereas SIS degraded most rapidly (10.5% ± 0.42%; p < 0.01 vs PAD) but provoked severe foreign body reactions (2.3-fold higher vs HAD at 13 weeks, p = 0.017). Notably, HAD uniquely promoted sustained M2-dominant macrophage polarization (CD206⁺/CD86⁺ ratio = 2.1 vs SIS = 0.7), which reduced inflammation and enhanced collagen remodeling (p < 0.05 vs SIS). Serum metabolomic analysis indicated that ECM mesh implantation induced a reprogramming of host amino acid metabolism, marked by a notable acceleration in L-methionine metabolism. The proposed integrated evaluation framework successfully identifies material-specific correlations among degradation behavior, immune response, and metabolic regulation, providing critical benchmarks for the rational design of immunomodulatory ECM meshes.

PMID 42168293
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