Global Bispecific Antibody Market To Witness Around 5 New Bispecific Antibodies Approval By 2029 Says Kuick Research
Delhi, March 17, 2024 (GLOBE NEWSWIRE) -- Global Bispecific Antibody Market Opportunity Insight 2029 Report Highlights:
-
Global Market Forecast Till 2029: > USD 36 Billion
-
Approved Bispecific Antibodies: 11
-
Yearly & Quarterly Sales Insight
-
Global & Regional Sales Insights
-
Insight On Bispecific Antibodies In Clinical Trials: > 600 Bispecific Antibodies
-
Global Bispecific Antibodies Clinical Trials By Company, Indication & Phase
-
Fast Track Approval, Orphan Designation & Priority Status Insights
-
Approved Bispecific Antibodies Pricing & Dosage Analysis
-
Top 30 Companies Developing Bispecific Antibodies Competitive Insight
-
800 Pages Clinical & Commercial Opportunity insight
Download Report:
https://www.kuickresearch.com/report-bispecific-antibody-market-bispecific-antibodies-market
Pidilizumab, formerly known as CT-011, is a monoclonal antibody under development, poised to revolutionize the landscape of cancer and infectious disease treatment. This humanized IgG monoclonal antibody is meticulously crafted to target the human inhibitory receptor programmed cell death 1 (PD-1), showcasing its potential as both an immune checkpoint inhibitor and an antineoplastic agent. Operating at the molecular level, pidilizumab exerts its effects by binding to PD-1, thereby thwarting the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). By disrupting this crucial signaling pathway, pidilizumab prevents the activation of PD-1 and its downstream cascades, consequently revitalizing immune function.
The ramifications of pidilizumab's action extend far beyond mere molecular interactions, as it holds the promise of reinstating immune surveillance against tumor cells. PD-1, a pivotal inhibitory receptor belonging to the B7-receptor family, is ubiquitously expressed on activated T-lymphocytes, B-cells, and NK cells. However, its activation by ligands serves as a roadblock to T-cell activation and effector function, thereby fostering tumor evasion from host immunity. Through its blockade of PD-1, pidilizumab facilitates the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs), empowering these immune warriors to launch a concerted attack against malignant cells.
Initially believed to primarily target the PD-1 immune checkpoint molecule, recent insights have shed light on pidilizumab's nuanced binding interactions. Contrary to initial assumptions, evidence now suggests that Delta-like ligand 1 (DLL1) serves as its primary binding target, with its binding to PD-1 relegated to non-glycosylated and hypoglycosylated forms of this molecule. This newfound understanding underscores the complexity of pidilizumab's mode of action, prompting further exploration into its molecular mechanisms and clinical implications.