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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

PubMedJournal of orthopaedic research : official publication of the Orthopaedic Research Society2026-07-24

Monitoring Progressive, Biologically Mediated Tendon Degeneration Using Quantitative Polarized Light Imaging.

Iannucci Leanne E LE, Lake Spencer P SP

Degenerative tendon tears are common, but mechanisms behind initiation and progression are not fully understood. There is a clear need to be able to track microstructural changes during progressive biological degradation to better understand degenerative tendon pathophysiology. The aim of this study was to evaluate the sensitivity of a snapshot Stokes polarimetry technique, quantitative polarized light imaging (QPLI), in monitoring the severity and progression of biologically mediated degeneration in tendon. Leveraging a collagenase mediated in vitro tendon digestion model, we assessed the effect of enzyme degradation on polarimetric outcomes from reflectance and transmission modes of QPLI, second harmonic generation (SHG) imaging, histology, and mechanical testing. Changes observed in reflectance mode QPLI (rQPLI) allowed for characterization of progression of degeneration at all digestion severities tested, whereas data acquired from transmission mode QPLI was only able to discern changes at the most severe digestion level. Outcomes from this study establish rQPLI as a powerful tool in the microstructural evaluation of musculoskeletal soft tissues, particularly in the context of monitoring progressive degradation. The findings from this study also highlight the potential multiscale nature of biological degeneration in tendon and emphasize the importance of better understanding these processes to inform regeneration and repair strategies.

PMID 42494122
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PubMedExperimental neurology2026-07-24

The LncRNA CRNDE/miR-152-3p/ROCK1 axis aggravates neurological deficits and neuroinflammation in intracerebral hemorrhage.

Xiao Junli J, Wang Ming M, Zuo Haiyan H, Yan WeiChen W

Intracerebral hemorrhage (ICH) is a fatal cerebrovascular disease. This study explored the intrinsic relationship between ICH and lncRNA CRNDE. Injecting the lentiviral interference vector (sh-CRNDE) into the ICH mice (induced by collagenase). Subsequently, the neurological deficits were evaluated through Garcia scoring, the corner turn test, and the water maze test. The levels of CRNDE and inflammatory factors in the brain tissue were detected by RT-qPCR and ELISA, respectively. In vitro experiments, microglia and neuronal cells were respectively cultured with hemoglobin and Hemin. Subsequently, the level of M1 polarization markers was detected by RT-qPCR. In neuronal cells, the proliferation activity was evaluated by CCK-8. The apoptosis level was comprehensively assessed based on the results of flow cytometry and the level of LDH. Finally, the effects of inhibiting the CRNDE/miR-152-3p axis on ROCK1 and the phenotype of ICH were re-verified in animal models and cell models. In ICH mice, inhibition of CRNDE prevented the neurological deficits and neuroinflammation. Blocking CRNDE also significantly alleviated the M1 polarization of microglia and the apoptosis of neuronal cells. CRNDE sponges miR-152-3p through the ceRNA mechanism and regulates ROCK1. Inhibition of miR-152-3p or overexpression of ROCK1 weakens the inhibitory effect of sh-CRNDE on neurological deficits, M1 polarization, and the apoptosis of neurons. Moreover, in cell models, inhibition of ROCK1 showed the same protective effect as CRNDE downregulation. In ICH, CRNDE upregulates ROCK1 by adsorbing miR-152-3p. This regulatory axis exacerbates neuroinflammation and neurofunctional disorders.

PMID 42492830
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PubMedCancer immunology research2026-07-24

Periductal Fibroblast Density Defines Lymphocyte Exclusion via a CD44-Dependent Stromal Checkpoint in Pancreatic Cancer.

Malchiodi Zoe X ZX, Lekan Alexander A AA, Suter Robert K RK, Deshpande Atul A et al.

Pancreatic ductal adenocarcinoma (PDAC) exhibits dense fibrosis and immune exclusion. While fibrosis has been studied globally and at the region-of-interest level, its impact on stromal-ductal architecture and immune cell localization remains unknown. Here, we establish cancer-associated fibroblast (CAF)-stratified ductal spatial architecture as a fundamental determinant of immune exclusion in PDAC. Focusing on malignant PDAC epithelial ductal regions, the critical interface where immune cells must access tumor epithelium, we demonstrate that periductal fibroblast organization dictates leukocyte proximity. Through integrative analysis of treatment-naïve patient samples from three independent cohorts - including imaging mass cytometry, multiplex immunohistochemistry, and single-cell RNA sequencing - we uncover that activated, pro-inflammatory leukocytes preferentially localize near malignant ducts in regions with low fibroblast density. Stratifying epithelial-ductal regions by CAF abundance reveal a graded constraint: increasing fibroblast content corresponds to reduced leukocyte-epithelial proximity and elevated collagen I deposition. Despite their exclusion in high-CAF ducts, leukocytes in low-CAF ducts retain functional competence. Mechanistically, ligand-receptor inference implicates collagen-CD44 signaling as an adhesion axis anchoring immune cells within fibroblast-rich zones. CD44 blockade augments natural killer cell motility in vitro, while enhancing lymphocyte collagenase activity through MMP14 overexpression promotes infiltration by overcoming αSMA+ CAF-mediated stromal barriers in vivo. Thus, by establishing ductal regions as critical spatial units of immune exclusion, these findings provide a framework for dissecting stromal-immune interactions, reveal targetable "stromal checkpoints", and provide complementary strategies to overcome CAF-driven barriers to leukocyte motility and infiltration in PDAC.

PMID 42497294
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PubMedJournal of Ayurveda and integrative medicine2026-07-22

Commiphora wightii and its formulations extenuate macrophage-mediated inflammatory pathology in osteoarthritis.

Srivastava Vanshika V, Raj Ritik R, Ganeshpurkar Ankit A, Kulkarni Priya P et al.

Osteoarthritis (OA) treatment often focuses on symptom management rather than addressing underlying inflammation and cartilage degeneration. In search of safer, long-term options, many patients turn to Ayurvedic remedies like Guggul (Commiphora wightii) and its formulations-Amritadi Guggul (AG) and Rasnadi Guggul (RG)-though biochemical validation remains limited. This study evaluates the immunomodulatory effects of standard guggulsterone extract (SGE), AG, and RG on synovial inflammation, mitochondrial stress, and complement activation, using the U937 monocyte cell line. Cells were stimulated with Phorbol 12-myristate 13 acetate (PMA) and treated with varying concentrations of the extracts. Anti-inflammatory effects were measured via mRNA expression of iNOS, MMP-1, MMP-13, and VEGF-1. Macrophage polarization markers (CD68, CD86, CD163), mitochondrial membrane potential (JC-1 assay), collagenase activity (gelatinase spot assay), and molecular docking with complement factor B (CFB) were also assessed. Results showed that SGE, AG, and RG significantly reduced nitric oxide and pro-inflammatory gene expression. Treatments suppressed M1 macrophage markers without promoting M2 differentiation. 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimi- dazolylcarbocyanine iodide (JC) - 1 assays indicated improved mitochondrial stability, while all formulations inhibited collagenase activity. Docking studies revealed strong interactions between guggulsterone and CFB, suggesting complement inhibition. These findings highlight the potential of Guggul and its formulations to modulate macrophage activity, reduce inflammation, and support joint preservation in OA. Though limited by the use of a monocyte-derived cell line, the study lays the groundwork for future validation in primary cells and in vivo models.

PMID 42485742
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PubMedTranslational stroke research2026-07-21

Targeting the Mechanosensitive Channel Piezo2 Alleviates Intracerebral Hemorrhage-induced Brain Injury by Modulating ER Stress.

Han Shuai S, Wang Zirui Z, Zhao Jihu J, Zheng Qiuyue Q et al.

Secondary brain injury (SBI) following intracerebral hemorrhage (ICH) is heavily driven by the mechanical compression of the expanding hematoma, yet how neurons transduce this physical force into pathological intracellular signals remains poorly understood. This study investigates the role of the mechanosensitive ion channel Piezo2 in ICH-induced SBI and its underlying molecular mechanisms. Using a collagenase-induced ICH mouse model and single-cell RNA sequencing analysis, we identified a marked upregulation of Piezo2 in perihematomal neurons. To determine its functional significance, we employed both genetic knockdown (shRNA) and pharmacological modulation with D-GsMTx4 in vivo. Modulation of Piezo2 significantly alleviated acute neurological deficits, reduced brain edema, and improved long-term cognitive performance in ICH mice. Mechanistically, we observed that the neuroprotective effects of Piezo2 inhibition were associated with an attenuation of neuronal endoplasmic reticulum (ER) stress. Specifically, inhibition of Piezo2 preserved ER ultrastructure, which was accompanied by a robust downregulation of the PERK/ATF4/CHOP signaling cascade markers. Collectively, our findings suggest that Piezo2 contributes to neuronal damage following ICH and that its modulation impacts ER stress. Targeting Piezo2 represents a novel experimental concept to mitigate secondary neurodegeneration associated with hematoma-induced mechanical strain, though extensive preclinical optimization is required before considering its clinical viability.

PMID 42479308
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-07-17

HD-tDCS Restores Perivascular AQP4 Polarization via PPARγ Modulation to Enhance Glymphatic Clearance After Intracerebral Hemorrhage in Mice.

Li Zhiming Z, Zhang Yingmei Y, Tong Qianqian Q, Gong Zhitao Z et al.

Impaired perivascular aquaporin 4 (AQP4) polarization and glymphatic dysfunction after intracerebral hemorrhage (ICH) may delay hematoma and perihematomal edema resolution. The effects of high-definition transcranial direct current stimulation (HD-tDCS) on glymphatic transport and recovery after ICH, as well as the underlying mechanisms, are investigated in a collagenase-induced mouse model. HD-tDCS (anodal stimulation, 0.1 mA, 10 min daily) significantly enhances cerebrospinal fluid influx, improves interstitial solute clearance, reduces intracerebral tracer retention, and increases drainage to the deep cervical lymph nodes, as assessed by in vivo two-photon imaging, contrast-enhanced MRI, and ex vivo tracer analysis. HD-tDCS also accelerates hematoma and edema resolution, reduces midline shift and diffusion abnormalities, and improves neurological outcomes. Mechanistically, ICH induces astrocytic proinflammatory activation together with impaired perivascular AQP4 polarization, whereas HD-tDCS upregulates peroxisome proliferator-activated receptor gamma (PPARγ), suppresses proinflammatory astrocyte activation, and restores perivascular AQP4 localization. Astrocyte-specific knockdown or pharmacologic inhibition of PPARγ attenuates HD-tDCS-induced AQP4 repolarization, glymphatic recovery, and neurological improvement. These findings indicate that HD-tDCS promotes hematoma and edema resolution after ICH in association with PPARγ-dependent astrocyte remodeling, AQP4 repolarization, and glymphatic restoration.

PMID 42467855
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