IL-15 agonists(Interleukin-15 agonists), PDL1 inhibitors(Programmed death-ligand 1 inhibitors), PDL2 inhibitors(Programmed cell death 1 ligand 2 inhibitors)

Therapeutic Areas

Neoplasms

Active Indication

Solid tumor

Inactive Indication-

Originator Organization

AKSO Biopharmaceutical, Inc.

Active Organization

AKSO Biopharmaceutical, Inc.

Huadong Medicine Co., Ltd.

Inactive Organization-

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

100 Clinical Results associated with AB002

100 Translational Medicine associated with AB002

100 Patents (Medical) associated with AB002

Literatures (Medical) associated with AB002

01 Jun 2023·Talanta

Coreactant-free electrochemiluminescence of polyfluorene nanoparticle coupling double quencher for β-amyloid1-42 detection

Article

Author: Yang, Guomin ; Xie, Jiaping ; Chen, Shihong ; Tan, Xingrong ; Yuan, Ruo

β-amyloid_1-42 (Aβ_1-42) is a humoral biomarker for early diagnosis of Alzheimer's disease (AD), and exists at a low level in human body. Its sensitive detection is very valuable. The electrochemiluminescence (ECL) assay of Aβ_1-42 has attracted special attention owing to high sensitivity and simple operation. However, currently reported ECL assays for Aβ_1-42 usually required the introduction of exogenous coreactants to improve the detection sensitivity. Introducing exogenous coreactants will lead to non-negligible repeatability and stability problems. This work exploited poly [(9,9-dioctylfluorenyl-2,7-diyl)-co-(1,4-benzo-{2,1',3}-thiadazole)] nanoparticles (PFBT NPs) as coreactant-free ECL emitters for detecting Aβ_1-42. The PFBT NPs, first antibody (Ab₁) and antigen Aβ_1-42 were successively assembled on glassy carbon electrode (GCE). Silica nanoparticles served as a carrier to grow polydopamine (PDA) in situ, and further assembled Au nanoparticles (Au NPs) and second antibody (Ab₂), producing the secondary antibody complex (SiO₂@PDA-Au NPs-Ab₂). With its assembly on the biosensor, the ECL signal decreased since both PDA and Au NPs could quench ECL emission from PFBT NPs. The limit of detection (LOD) of 0.55 fg/mL and limit of quantification (LOQ) of 37.45 fg/mL for Aβ_1-42 were obtained. PFBT NPs coupling dual-quencher PDA-Au NPs created an excellent ECL system for bioassays, and constructed a sensitive analytical method for Aβ_1-42.

01 Nov 2020·Molecular Cancer TherapeuticsQ2 · MEDICINE

Dual Mechanisms of Novel CD73-Targeted Antibody and Antibody–Drug Conjugate in Inhibiting Lung Tumor Growth and Promoting Antitumor Immune-Effector Function

Q2 · MEDICINE

Article

Author: Wang, Xin ; Yu, Ker ; Jin, Rui ; Ren, Zhiqiang ; Ma, Lanping ; Liu, Liang ; Shen, Jingkang ; Cong, Ying ; Zhang, Xuesai ; Xing, Yun ; Meng, Tao ; Pei, Jinpeng

AbstractAlthough tyrosine kinase inhibitor therapy and immunotherapy have significantly improved lung cancer management, many patients do not benefit or become resistant to treatment, highlighting the need for novel treatments. We found elevated CD73 expression to be prevalent in non–small cell lung cancer (NSCLC) including those harboring the RAS- or RTK (EGFR, EML4-ALK) oncogenes. CD73 expression is enriched closely with the transcriptome signature of epithelial–mesenchymal transition and the immune-tolerant tumor microenvironment, which are increasingly relevant for disease progression and therapy resistance. We developed two novel series of CD73 antibody, Ab001/Ab002 and humanized version Hu001/Hu002, which demonstrated high CD73 binding affinity, potent enzyme inhibition, and efficiently protected effector T lymphocyte function from adenosine/cancer-imposed toxicity. Hu001/Hu002 inhibited growth of RAS-mutant NSCLC tumors in mice via enhanced antibody-dependent cell-mediated cytotoxicity and multifaceted remodeling of the tumor immune environment, reflecting diminished levels of tumor-associated macrophages, myeloid-derived suppressor cells, and tumor vasculature. A novel MMAE-conjugated CD73-ADC (Hu001–MMAE) elicited potent cytotoxicity against CD73-high expressing tumor cells (IC50<0.1 nmol/L) and suppressed in vivo growth of multiple NSCLC and glioma tumors, including the RAS-mutant models [minimum effective dose <1 mg/kg]. Treatment with CD73–ADC triggered a robust intratumoral accumulation of proinflammatory macrophages and activated dendritic cells (DC), which were not observed with naked CD73 antibody or standard chemotherapy. Studies with human PBMC-derived systems confirmed CD73-ADC as fully functional in protecting effector T cells and stimulating DCs thus providing dual benefits in killing CD73-high tumors and improving cancer immunity response. These results warrant clinical investigation of CD73-targeted antibody and ADC for treating advanced lung cancer.

27 Feb 2020·BloodQ1 · MEDICINE

The protein C activator AB002 rapidly interrupts thrombus development in baboons

Q1 · MEDICINE

Article

Author: Verbout, Norah G. ; Hinds, Monica T. ; Lorentz, Christina U. ; Markway, Brandon D. ; McCarty, Owen J. T. ; Wood, David C. ; Shatzel, Joseph J. ; Pelc, Leslie A. ; Gruber, András ; Tucker, Erik I. ; Wallisch, Michael ; Di Cera, Enrico

AbstractAlthough thrombin is a key enzyme in the coagulation cascade and is required for both normal hemostasis and pathologic thrombogenesis, it also participates in its own negative feedback via activation of protein C, which downregulates thrombin generation by enzymatically inactivating factors Va and VIIIa. Our group and others have previously shown that thrombin’s procoagulant and anticoagulant activities can be effectively disassociated to varying extents through site-directed mutagenesis. The thrombin mutant W215A/E217A (WE thrombin) has been one of the best characterized constructs with selective activity toward protein C. Although animal studies have demonstrated that WE thrombin acts as an anticoagulant through activated protein C (APC) generation, the observed limited systemic anticoagulation does not fully explain the antithrombotic potency of this or other thrombin mutants. AB002 (E-WE thrombin) is an investigational protein C activator thrombin analog in phase 2 clinical development (clinicaltrials.gov NCT03963895). Here, we demonstrate that this molecule is a potent enzyme that is able to rapidly interrupt arterial-type thrombus propagation at exceedingly low doses (<2 µg/kg, IV), yet without substantial systemic anticoagulation in baboons. We demonstrate that AB002 produces APC on platelet aggregates and competitively inhibits thrombin-activatable fibrinolysis inhibitor (carboxypeptidase B2) activation in vitro, which may contribute to the observed in vivo efficacy. We also describe its safety and activity in a phase 1 first-in-human clinical trial. Together, these results support further clinical evaluation of AB002 as a potentially safe and effective new approach for treating or preventing acute thrombotic and thromboembolic conditions. This trial was registered at www.clinicaltrials.gov as #NCT03453060.

100 Deals associated with AB002

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Solid tumor	Preclinical	CN	Huadong Medicine Co., Ltd.	01 Jul 2022
Solid tumor	Preclinical	US	AKSO Biopharmaceutical, Inc.	01 Jul 2022

Clinical Result

Indication

Phase

Evaluation

View All Results

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Chat with Hiro

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


No Data

AB002

Overview

Basic Info

Related

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation