Request Demo

Last update 08 May 2025

CTSB x CTSL

Last update 08 May 2025

Basic Info

Related Targets

CTSBCTSL

Drugs associated with CTSB x CTSL

212-148

Target

CTSB x CTSL x TMPRSS2

Mechanism

CTSB inhibitors [+2]

Active Org.

Shanghaitech University

Originator Org.

Shanghaitech University

Active Indication

COVID-19

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AM-4299a

Target

CTSB x CTSL

Mechanism

CTSB inhibitors [+1]

Active Org.-

Originator Org.

Asahi Kasei Corp.

Active Indication-

Inactive Indication

Osteoporosis [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WF-14861

Target

CTSB x CTSL

Mechanism

CTSB inhibitors [+1]

Active Org.-

Originator Org.

Fujisawa Pharmaceutical Co., Ltd.

Active Indication-

Inactive Indication

Arthritis

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CTSB x CTSL

100 Translational Medicine associated with CTSB x CTSL

0 Patents (Medical) associated with CTSB x CTSL

689

Literatures (Medical) associated with CTSB x CTSL

01 Jul 2025·Journal of Invertebrate Pathology

Infection of two cestode larvae, Nybelinia enterika sp. nov. and Phoreiobothrium sp. in oval squid Sepioteuthis lessoniana species complex

Article

Author: Zifcakova, Lucia ; Nakamura, Shinichi ; Zoral, Mehmet Arif ; Miller, Jonathan ; Lajbner, Zdenek

Recently, oval squid of Sepioteuthis lessoniana species complex has gained importance in aquaculture due to its successful breeding in semi-intensive and intensive aquaculture systems. However, there is a lack of information regarding pathogens and diseases that can affect this species, prompting the need for further research. Two cestode species, Nybelinia enterika sp. nov. and Phoreiobothrium sp., were identified as members of the Trypanorhyncha and Onchoproteocephalidea orders, respectively, using both morphological and molecular diagnostic markers in wild-caught oval squids (Sepioteuthis lessoniana sp.1, S. lessoniana sp.2, S. lessoniana sp.3). These cestode species were found to use the oval squids as intermediate hosts. In histopathology samples, the infected squid with N. enterika was surrounded by numerous hemocytes in the infected area. In the genomes of both cestode species, we identified multiple genes for enzymes involved in cephalopod tissue degradation, such as cysteine proteases including cathepsin-L, cathepsin-D, cathepsin-A, cathepsin-B, cathepsin-K, and cathepsin-S. These enzymes potentially help the parasites manipulate the squid immune system and neutralize squid hemocytes. The detection of these parasites in wild squid populations, with 100% prevalence in Okinawa, is concerning as the effect of these parasites on human consumers' health remains unknown. However, our research demonstrated that fully cultured squid remain completely cestode parasite-free, indicating they are more likely to meet the highest standards for food safety and quality.

01 Apr 2025·Ecotoxicology and Environmental Safety

Alumina nanoparticles induce learning and memory impairment in a particle size-dependent and time-dependent manner

Article

Author: Jia, Lina ; Zhang, Qinli ; Niu, Qiao ; Guo, Weiwei ; Zhang, Ying ; Ge, Cuicui ; Qin, Xiujun ; Wang, Zhiwu

The study investigates the influence of alumina nanoparticles (Al₂O₃ NPs) at varying sizes on the learning and memory of adult ICR mice over different exposure durations. The mice were administered saline or Al₂O₃ nanoparticles of 10μm, 50 nm, and 13 nm via nasal drip. Following administration, the Morris water maze test was conducted, along with assessments of inflammation, oxidative stress, hippocampal histopathology, and cell death-related proteins. Initially, after acute exposure, a trend emerged where learning and memory gradually declined as nanoparticle size decreased, with the most significant impact observed in the 13 nm Al₂O₃ group. Upon chronic exposure, there was a significant decline in learning and memory within the Al₂O₃ NPs groups compared to other groups, accompanied by neuronal loss, swelling, light staining, and disorganization. Concurrently, levels of TNF-α and IL-1β within 7 days, MDA after 7 days, and death-related proteins such as Cathepsin-B, c-caspase3, LC3-II, Beclin1, RIP, and Cathepsin-L showed a linear increase, while SOD and GSH-PX activity steadily decreased. Over time, learning capability decreased, correlating with a sharp reduction in TNF-α and SOD activity, a gradual increase in MDA, c-caspase3, and Beclin1 levels in the Al₂O₃ NPs group, as well as elevated Cathepsin-L, LC3-II, and RIP levels in the 13 nm Al₂O₃ group. Consequently, Al₂O₃ NPs significantly impaired learning and memory in a particle size-dependent manner through initial inflammation and oxidative stress after acute exposure, and time-dependent impairment via escalating oxidative stress and neuronal death.

11 Mar 2025·Proceedings of the National Academy of Sciences

Inhibition of amyloid beta oligomer accumulation by NU-9: A unifying mechanism for the treatment of neurodegenerative diseases

Article

Author: Zhu, Wei ; Kranz, Daniel L. ; Nowar, Raghad ; Silverman, Richard B. ; Viola, Kirsten L. ; Huang, Weijian ; Johnson, Elizabeth A. ; Klein, William L. ; Zhou, Sihang ; Bicca, Maíra A.

Protein aggregation is a hallmark of neurodegenerative diseases, which connects these neuropathologies by a common phenotype. Various proteins and peptides form aggregates that are poorly degraded, and their ensuing pathological accumulation underlies these neurodegenerative diseases. Similarities may exist in the mechanisms responsible for the buildup of these aggregates. Therefore, therapeutics designed to treat one neurodegenerative disease may be beneficial to others. In ALS models, the compound NU-9 was previously shown to block neurodegeneration produced by aggregation-inducing mutations of SOD-1 and TDP-43 [B. Genç et al., Clin. Transl. Med.11 , e336 (2021)]. Here, we report that NU-9 also prevents the accumulation of amyloid beta oligomers (AβOs), small peptide aggregates that are instigators of Alzheimer’s disease neurodegeneration [M. Tolar et al., Int. J. Mol. Sci.22 , 6355 (2021)]. AβO buildup was measured by immunofluorescence imaging of cultured hippocampal neurons exposed to exogenous monomeric Aβ. In this model, AβO buildup occurs via cathepsin L- and dynamin-dependent trafficking. This is prevented by NU-9 through a cellular mechanism that is cathepsin B- and lysosome-dependent, suggesting that NU-9 enhances the ability of endolysosomal trafficking to protect against AβO buildup. This possibility is strongly supported by a quantitative assay for autophagosomes that shows robust stimulation by NU-9. These results contribute additional understanding to the mechanisms of protein aggregation and suggest that multiple neurodegenerative diseases might be treatable by targeting common pathogenic mechanisms responsible for protein aggregation.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis