Delving into the Latest Updates on AbGenomics B.V Taiwan Branch with Synapse

Overview

Basic Info

Introduction

The Taiwan Branch of AbGenomics B.V is a biopharmaceutical subsidiary focused on creating groundbreaking antibody therapies for cancer and inflammatory diseases. As part of AbGenomics Corporation, an international biotech firm with a presence in both the USA and Asia, they focus their research on innovative, top-class antibody drugs, drawing from a wealth of knowledge in immunology, oncology, and antibody technology. Established in 2003, one of their main goals is to create inventive treatments for diseases which currently lack sufficient medical solutions, with the aim of enhancing global health and well-being.

This study is to define the safety profile and to determine the Maximal tolerated dose regimen and preliminary efficacy of AbGn-107 administered every 14 days (Q2W regimen) or 28 days (Q4W regimen) in patients with chemo-refractory locally advanced, recurrent or metastatic gastric, colorectal, pancreatic or biliary cancer.

Start Date24 Apr 2017

Sponsor / Collaborator

AbGenomics B.V Taiwan Branch

NCT02694770 / WithdrawnPhase 2

A Phase II Study of Neihulizumab vs "Conventional Treatment" to Treat Steroid-refractory Acute Graft-vs-host Disease (Sr-aGvHD) in Patients Undergoing Allogeneic Hematopoietic Cell Transplantation

This study is to assess the efficacy of Neihulizumab versus "conventional therapy" and to evaluate safety, pharmacokinetics and immunogenicity in treating steroid-refractory acute Graft-vs-Host Disease

Start Date01 Jul 2016

Sponsor / Collaborator

AbGenomics B.V Taiwan Branch

NCT02436460 / TerminatedPhase 1

A Phase Ib Treatment Trial Using AbGn-168H to Treat Steroid Refractory Acute Graft-vs.-Host Disease (aGVHD) in Patients Undergoing Allogeneic Hematopoietic Cell Transplantation

This study is to establish the safety, determine if there is an improvement in steroid refractory acute graft-vs-host disease (aGvHD) compared to historical cohorts, and determine the changes of aGvHD-associated T-cell clones in patients with steroid-refractory aGVHD following allogeneic hematopoietic cell transplantation administered AbGn-168H once weekly for 4 weeks.

Start Date01 May 2015

Sponsor / Collaborator

AbGenomics B.V Taiwan Branch

100 Clinical Results associated with AbGenomics B.V Taiwan Branch

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0 Patents (Medical) associated with AbGenomics B.V Taiwan Branch

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1

Literatures (Medical) associated with AbGenomics B.V Taiwan Branch

Increasing endogenous PPARγ ligands improves insulin sensitivity and protects against diet-induced obesity without side effects of thiazolidinediones

Author: Ke, Yi-Yu ; Huang, Jing-Yong ; Tsou, Lun ; Hwang, Juey-Jen ; Hung, Fu-Hsin ; Yang, Wei-Shun ; Lee, Hsiao-Lin ; Tseng, Yu-Hua ; Chiu, Chu-Hsuan ; Liu, Bi-Yu ; Lin, Shih-Yao ; Hung, Ming-Shiu ; Li, Fu-An ; Nong, Jiun-Yi ; Chang, Yi-Cheng ; Chen, Tzu-Yu ; Yeh, Teng-Kuang ; Chen, Shih-Yi ; Hsieh, Meng-Lun ; Kao, Fang-Chi ; Chou, Ya-Wen ; Hsu, Chih-Neng ; Chuang, Lee-Ming ; Hee, Siow-Wey ; Tai, Chi-Ming ; Chen, Yet-Ran ; Cheng, Ting-Jen ; Shih, Yvonne ; Cheng, Jamie

AbstractInsulin resistance and obesity are pivotal features of type 2 diabetes mellitus. Peroxisome proliferator-activated receptor γ (PPARγ) is a master transcriptional regulator of systemic insulin sensitivity and energy balance. The anti-diabetic drug thiazolidinediones are potent synthetic PPARγ ligands and insulin sensitizers with undesirable side effects including increased adiposity, fluid retention, and osteoporosis, which limit their clinical use. We and others have proved that 15-keto-PGE2 is an endogenous natural PPARγ ligand. 15-keto-PGE2 is catalyzed by prostaglandin reductase 2 (PTGR2) to become inactive metabolites. We found that 15-keto-PGE2 level is increased in Ptgr2 knockout mice. Ptgr2 knockout mice were protected from diet-induced obesity, insulin resistance, and hepatic steatosis without fluid retention nor reduced bone mineral density. Diet-induced obese mice have drastically reduced 15-keto-PGE2 levels compared to lean mice. Administration of 15-keto-PGE2 markedly improved insulin sensitivity and prevented diet-induced obesity in mice. We demonstrated that 15-keto-PGE2 activates PPARγ through covalent binding to its cysteine 285 residue at helix 3, which restrained its binding pocket between helix 3 and β-sheets of the PPARγ ligand binding domain. This binding mode differs from the helix12-dependent binding mode of thiazolidinediones. We further identified a small-molecule PTGR2 inhibitor BPRPT245, which interferes the interaction between the substrate-binding sites of PTGR2 and 15-keto-PGE2. BPRPT245 increased 15-keto-PGE2 concentration, activated PPARγ, and promoted glucose uptake in adipocytes. BPRPT245 also prevented diet-induced obesity, improved insulin sensitivity and glucose tolerance, lowers fasting glucose without fluid retention and osteoporosis. In humans, reduced serum 15-keto-PGE2 levels were observed in patients with type 2 diabetes compared with controls. Furthermore, serum 15-keto-PGE2 levels correlate inversely with insulin resistance and fasting glucose in non-diabetic humans. In conclusion, we identified a new therapeutic approach to improve insulin sensitivity and protect diet-induced obesity through increasing endogenous natural PPARγ ligands without side effects of thiazolidinediones.

100 Deals associated with AbGenomics B.V Taiwan Branch

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100 Translational Medicine associated with AbGenomics B.V Taiwan Branch

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Pipeline

Pipeline Snapshot as of 25 Nov 2024

The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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Current Projects

Drug(Targets)	Indications	Global Highest Phase

Neihulizumab ( PSGL-1 )	Steroid Refractory Graft Versus Host Disease More	Discontinued
AbGn-107 ( Lewis-A x Tubulin )	Stomach Cancer More	Discontinued
AbGn-7 ( Lewis-A )	Advanced Malignant Solid Neoplasm More	Pending