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Last update 08 May 2025

BCAN

Last update 08 May 2025

Basic Info

Synonyms

BCAN, BEHAB, Brain-enriched hyaluronan-binding protein

+ [5]

Introduction

May play a role in the terminally differentiating and the adult nervous system during postnatal development. Could stabilize interactions between hyaluronan (HA) and brain proteoglycans.

Drugs associated with BCAN

BTP-7-CPT

Target

BCAN x Top I

Mechanism

BCAN modulators [+1]

Active Org.

Shaanxi University of Traditional Chinese Medicine

Originator Org.

Shaanxi University of Traditional Chinese Medicine

Active Indication

Glioma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BTP-7

Target

BCAN

Mechanism

BCAN modulators

Active Org.

Harvard Medical School [+1]

Originator Org.

Harvard Medical School

Active Indication

Glioma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1280

Target

BCAN x Chondroitin sulfate proteoglycans

Mechanism

BCAN modulators [+1]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with BCAN

100 Translational Medicine associated with BCAN

0 Patents (Medical) associated with BCAN

315

Literatures (Medical) associated with BCAN

01 May 2025·Pain

Formation of perineuronal nets within a thalamocortical circuit shapes mechanical and thermal pain thresholds in mice with neuropathic pain

Article

Author: Battaglia, Giuseppe ; Ginerete, Roxana Paula ; Zampini, Gloria ; Imbriglio, Tiziana ; Nicoletti, Ferdinando ; Mascio, Giada ; Bruno, Valeria ; Castaldi, Sonia ; Cannella, Milena ; Liberatore, Francesca ; Bucci, Domenico ; Ceccherelli, Alessia ; Notartomaso, Serena

AbstractWe moved from the hypothesis that perineuronal nets (PNNs), which are condensed structures of the extracellular matrix surrounding GABAergic interneurons in the forebrain, contribute to mechanisms of maladaptive neuronal plasticity underlying chronic pain. Here, we found that the density of PNNs labelled with the lectin Wisteria Floribunda Agglutinin (WFA) increased in the contralateral somatosensory cortex (SSC), medial prefrontal cortex (mPFC), reticular thalamic nucleus (RTN), and insular cortex of mice developing neuropathic pain in response to unilateral chronic constriction injury of the sciatic nerve. These regions are involved in neuronal circuits underlying perception, sufferance, embodiment, and top-down control of pain. At least in the SSC and mPFC, the increased density of WFA+ PNNs was associated with an up-regulation of the proteoglycans, brevican and neurocan, as shown by immunoblot analysis. Enzymatic degradation of PNNs caused by local infusion of chondroitinase ABC in the contralateral SSC or RTN enhanced both mechanical and thermal pain thresholds in chronic constriction injury mice. In contrast, siRNA-induced knock-down of the PNN-degrading enzyme, type-9 matrix metalloproteinase (MMP-9), in the SSC or RTN lowered pain thresholds in sham-operated mice. These data, combined with our previous findings obtained in mice with chronic inflammatory pain, suggest that an enhanced formation/reduced degradation of WFA+ PNNs in regions of the pain matrix is associated with different types of chronic pain and may drive mechanisms of nociceptive sensitization leading to reduced mechanical and thermal pain thresholds.

01 Apr 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Melatonin enhances neurogenesis and neuroplasticity in long-term recovery following cerebral ischemia in mice

Article

Author: Yilmaz, Bayram ; Kilic, Ertugrul ; Celik, Ulkan ; Beker, Merve ; Elibol, Birsen ; Caglayan, Ahmet Burak ; Altug, Burcugul ; Beker, Mustafa Caglar

The important therapeutic role of melatonin in neuropathological conditions is underscored by a broad array of studies, many of which elucidated its neuroprotective properties. Yet, our scientific knowledge still needs several approaches to uncover molecular mechanisms. In this study, we contextually modelled cerebral ischemia through transient intraluminal middle cerebral artery occlusion. Melatonin was administered via an intraperitoneally placed mini osmotic pump, and released periodically from 3 days post-ischemia (dpi) to 56 dpi. We conferred several lines of evidence to address the fundamental questions about melatonin's cytoprotective functions after cerebral ischemia. We demonstrated that melatonin assisted post-ischemic neuro-restoration and micro-vascularization. In addition, it restricted glial scar formation, which interferes with neuronal interactions and stands as a barrier against plasticity. Even more interestingly, axonal plasticity, which was studied on the pyramidal tract using an anterograde tract tracer, proved the role of melatonin in remodeling across the injury site. In addition, plasticity-associated membrane-localized proteins, ephrin b1, ephrin b2, brevican, and versican were also modulated by melatonin. These findings suggested that melatonin orchestrated neurological recovery which was accompanied by molecular alterations resulting in cellular and extracellular structural changes. Based on the molecular signatures, ipsilesional and contralesional brain tissues were finely tuned by melatonin to compensate the loss after ischemia. Accordingly, neurological improvements correlated with the brain's molecular changes over time. It was suggested that melatonin enabled neuronal recovery by regulating neurogenesis and neuroplasticity in long term.

01 Mar 2025·Brain Research Bulletin

Association of cortical macrostructural and microstructural changes with cognitive performance and gene expression in subcortical ischemic vascular disease patients with cognitive impairment

Article

Author: Liu, Xiaoshuang ; Huang, Jing ; Cheng, Runtian ; Luo, Tianyou ; Chen, Li

OBJECTIVEPrevious researches have demonstrated that patients with subcortical ischemic vascular disease (SIVD) exhibited brain structure abnormalities. However, the cortical macrostructural and microstructural characteristics and their relationship with cognitive scores and gene expression in SIVD patients remain largely unknown.METHODSThis study collected 3D-T1 and diffusion tensor imaging data from 30 SIVD patients with cognitive impairment (SIVD-CI) and 32 normal controls. The between-group comparative analyses of cortical thickness, area, volume, local gyrification index (LGI), and mean diffusivity (MD) were conducted with a general linear model. Moreover, the associations between the significant neuroimaging values and the cognitive scores and gene expression values from Allen Human Brain Atlas database were evaluated using partial least squares regression and partial correlation analysis.RESULTSSIVD-CI patients showed significant decreases in cortical thicknesses across 18 regions, cortical volumes across three regions, and cortical LGI across five regions, as well as significant increases in cortical MD across five regions (P < 0.05). The significantly reduced cortical thicknesses of the right insula, left superior temporal gyrus, left central anterior gyrus, and left caudal anterior cingulate cortex, as well as the significantly reduced cortical LGI in left caudal anterior cingulate cortex, were significantly positively correlated with different cognitive scores (P < 0.05). Furthermore, the abnormal cortical structural indicators were found to be significantly related to nine risk genes (VCAN, APOE, EFEMP1, SALL1, BCAN, KCNK2, EPN2, DENND1B and XKR6) (P < 0.05).CONCLUSIONSThe specific cortical structural damage may be related to specific cognitive decline and specific risk genes in SIVD-CI patients.

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