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Last update 23 Jan 2025

DSG2

Last update 23 Jan 2025

Basic Info

Synonyms

Cadherin family member 5, CDHF5, desmoglein 2

+ [3]

Introduction

Component of intercellular desmosome junctions. Involved in the interaction of plaque proteins and intermediate filaments mediating cell-cell adhesion.

Drugs associated with DSG2

Adze-1.17.C.4.11

Target

CD46 x DSG2

Mechanism

CD46 inhibitors [+1]

Active Org.

Adze Biotechnology, Inc.Startup

Originator Org.

Adze Biotechnology, Inc.Startup

Active Indication

Glandular and Epithelial Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

KBA-1704

Target

DSG2

Mechanism

DSG2 inhibitors

Active Org.

Kling Biotherapeutics BVStartup

Originator Org.

Kling Biotherapeutics BVStartup

Active Indication

Colonic Cancer [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2023081674

Patent Mining

Target

DSG2

Mechanism-

Active Org.

ARVADA Therapeutics, Inc.

Originator Org.

ARVADA Therapeutics, Inc.

Active Indication

Cardiovascular Diseases [+4]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with DSG2

CTRI/2024/07/070006

/ Not yet recruitingPhase 3IIT

Comparative Evaluation of Efficacy of the Novel PRP Loop with Opus Loop for Anterior EnMasse Retraction in Angles Class I Deweys Type 2 Malocclusion A Single Blinded Randomized Clinical Trial. - NIL

Start Date01 Aug 2024

Sponsor / Collaborator-

100 Clinical Results associated with DSG2

100 Translational Medicine associated with DSG2

0 Patents (Medical) associated with DSG2

627

Literatures (Medical) associated with DSG2

01 Jan 2025·Heart Rhythm

Distribution of myocardial fibrosis in patients with nonischemic cardiomyopathy and ventricular tachycardia based on genetic variant

Article

Author: Tandri, Harikrishna ; Stevenson, William ; Weinand, Nicholas ; Hu, Tiffany ; Richardson, Travis ; Hasegawa, Kanae ; Kanagasundram, Arvind

BACKGROUNDMany genetic nonischemic dilated cardiomyopathies (NICMs) cause ventricular tachycardias (VTs) originating from scar substrate identified as areas of low electrogram voltage. Substrate locations vary, and the causes of scar are not well defined.OBJECTIVEThis study evaluated VT substrate locations in genetic NICM patients undergoing VT ablation to evaluate spatial relationships between specific variants and substrate locations.METHODSIn this retrospective case series analysis, 32 patients (aged 55 ± 16 years; 94% male; left ventricular ejection fraction, 34% ± 13%) with genetic NICM referred for VT ablation between October 2018 and November 2022 at a single medical center were evaluated. Scar locations were defined as areas of low unipolar or bipolar voltage.RESULTSOf the 32 patients evaluated, mutations in TTN (n = 11), LMNA (n = 6), PKP2 (n = 5), MYBPC3 (n = 3), DSP (n = 2), TTR (n = 1), FLNC (n = 1), AGL (n = 1), DES (n = 1), and DSG2 (n = 1) were observed. Substrates associated with mutations in TTN were observed only in basal subregions, predominantly anterior (100%) and septal (50%) regions. LMNA mutations were associated with fibrosis in mid inferolateral (60%) and apical inferolateral (60%) regions. Substrate location for individuals with PKP2 mutations was solely observed in the right ventricle, predominantly basal inferolateral regions.CONCLUSIONUnderstanding spatial relationships between genetic variants causing NICM and VT substrate locations can help lead to generalizable regions in patients with genetically related NICM presenting in VT, which can be investigated during ablation procedures.

01 Jan 2025·Pathology - Research and Practice

The phenotype of necrotizing enterocolitis correlates with distinct changes of intestinal junctional proteins

Article

Author: Niklas, Carolin ; Bartfeld, Sina ; Burkard, Natalie ; Hiller, Grit GR ; Härtel, Christoph ; Hörner, Marius ; Glaser, Kirsten ; Hiller, Grit Gr ; Meyer, Thomas ; Ernestus, Karen ; Schlegel, Nicolas ; Germer, Christoph-Thomas ; Kollmann, Catherine

Necrotizing enterocolitis (NEC) is a major cause of mortality in preterm infants. Its pathophysiology remains poorly understood but intestinal epithelial barrier dysfunction contributes to the disease. We characterized junctional proteins in intestinal specimens from preterm infants. Samples from 27 patients with NEC and 20 patients with focal intestinal perforation (FIP) from the center of the specimens (affected) or the macroscopically healthy resection margins whenever available (non-affected) were collected. NEC patients displayed higher mortality and more commonly occurrence of impaired glucose homeostasis, patent ductus arteriosus, anemia and antibiotic treatment compared to FIP patients. Discrimination between NEC and FIP was not possible in affected areas based on H.E. staining using a newly developed scoring system. Immunofluorescence revealed reduced Claudin-3 in affected NEC samples and decreased Claudin-4 in affected FIP and all NEC samples. E-cadherin and Desmoglein-2 were reduced in a subgroup of the affected NEC samples. Plakophilin-2 was decreased in intestine affected by FIP and unaffected intestine in patients with NEC. In affected areas of NEC, Plakophilin-2 was completely lost. Plakoglobin reduction in affected NEC samples correlated with poor survival. This study provides novel insights into changes of junctional proteins in NEC, suggesting Claudin-3 and Plakophilin-2 as diagnostic markers to differentiate FIP from NEC and reduced Plakoglobin as a prognostic marker.

31 Dec 2024·Emerging Microbes & Infections

Neutralizing monoclonal antibodies protect against human adenovirus type 55 infection in transgenic mice and tree shrews

Article

Author: Liu, Yutong ; He, Jun ; Zhang, Xiaoyan ; Li, Zhengfeng ; Wu, Weixuan ; Qu, Linbing ; Feng, Ying ; Chen, Ling ; Zhou, Rong ; Li, Xiao ; Liu, Xinglong ; Sun, Xikui ; Ye, Xianmiao ; Wang, Nana ; Zhou, Zhichao ; Su, Wan ; Feng, Liqiang ; Zheng, Yali ; Liu, Wenkuan ; Wang, Wei

Re-emerging human adenovirus type 55 (HAdV55) has become a significant threat to public health due to its widespread circulation and the association with severe pneumonia, but an effective anti-HAdV55 agent remains unavailable. Herein, we report the generation of macaque-derived, human-like monoclonal antibodies (mAbs) protecting against HAdV55 infection with high potency. Using fluorophore-labelled HAdV55 virions as probes, we isolated specific memory B cells from rhesus macaques (Macaca mulatta) that were immunized twice with an experimental vaccine based on E1-, E3-deleted, replication-incompetent HAdV55. We cloned a total of 19 neutralizing mAbs, nine of which showed half-maximal inhibitory concentrations below 1.0 ng/ml. These mAbs recognized the hyper-variable-region (HVR) 1, 2, or 7 of viral hexon protein, or the fibre knob. In transgenic mice expressing human desmoglein-2, the major cellular receptor for HAdV55, a single intraperitoneal injection with hexon-targeting mAbs efficiently prevented HAdV55 infection, and mAb 29C12 showed protection at a dose as low as 0.004 mg/kg. Fibre-targeting mAb 28E8, however, showed protection only at a dose up to 12.5 mg/kg. In tree shrews that are permissive for HAdV55 infection and disease, mAb 29C12 effectively prevented HAdV55-caused pneumonia. Further analysis revealed that fibre-targeting mAbs blocked the attachment of HAdV55 to host cells, whereas hexon-targeting mAbs, regardless of their targeting HVRs, mainly functioned at post-attachment stage via inhibiting viral endosomal escape. Our results indicate that hexon-targeting mAbs have great anti-HAdV55 activities and warrant pre-clinical and clinical evaluation.

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DSG2

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