Atypical Chemokine Receptor 3 Market Size, Share, Industry, Forecast and outlook (2024-2031)

Global Atypical Chemokine Receptor 3Market is Segmented  By Type (CCX-650, JT-07POL-6926, CCX-771Other), By Application (Atherosclerosis, Autoimmune Disorders, Crohn’s Disease, Others), and By Region (North America, Latin America, Europe, Asia Pacific, Middle East, and Africa) – Share, Size, Outlook, and Opportunity Analysis, 2024-2031

Atypical Chemokine Receptor 3 Market Overview

The Global "Atypical Chemokine Receptor 3 Market" size is estimated to reach at a high CAGR during the forecast period 2024-2031

The atypical chemokine receptor 3 (ACKR3) binds to the chemokines CXCL11 and CXCL12 and communicates solely via -arrestin-mediated pathways without activating canonical G-protein signaling. Because this receptor is upregulated in many cancers, it could be used as a drug target.

Atypical Chemokine Receptor 3 Market Scope

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Atypical Chemokine Receptor 3 Market Dynamics

The factors driving the market arethe emerging roles of atypical chemokine receptor 3.

The emerging roles of atypical chemokine receptor 3 are expected to dominate the market growth in the forecast period

The discovery that atypical chemokine receptors (ACKRs) can initiate alternative signaling pathways rather than classical G-protein coupled receptor (GPCR) signaling has altered the understanding of chemokine receptors and their roles in chemotactic response modulation. The ACKR family has grown over time as new functions and roles in various pathophysiological conditions have been discovered. The extent to which these receptors regulate normal physiology is still expanding. Atypical chemokine receptor 3 (ACKR3) is important in mediating normal functions such as cardiac development and cortical neuron migration.

CXCL12 and CXCL11 are chemokines that ACKR3 binds. Endothelial cells, some hematopoietic cells, mesenchymal cells, neurons, and astrocytes all express ACKR3. By forming heterodimers with CXCR4, ACKR3 can internalize CXCL12 and modulate CXCR4 expression and signaling.ACKR3/CXCR7 has been found on memory B cells and bone, brain, heart, and kidney in mammals. It has been demonstrated that it functions as a novel coreceptor for several immunodeficiency virus strains that infect brain-derived cells. In terms of function, ACKR3 acts as a scavenger receptor for a wide range of opioid peptides, particularly enkephalins and dynorphins, reducing their availability for classical opioid receptors.

Limitations of atypical chemokine receptor 3 are expected to hamper the market growth

In breast cancer, ACKR3 promotes cell growth by inducing ERK1/2 phosphorylation and inhibiting apoptosis. ACKR3 forms heterodimers with EGFR in breast and prostate cancer and stimulates its signaling, promoting tumor-cell proliferation in a ligand-independent manner. The use of an ACKR3 antagonist in lung cancer inhibits tumor growth. TGF-1 was also found to increase ACKR3 expression in lung adenocarcinoma, promoting tumor growth, and its expression correlates with lower patient survival rates. Together with CXCR4, ACKR3 expression is associated with a poor prognosis in renal cell carcinoma; in this tumor, ACKR3 promotes tumor growth by activating the mTOR pathway.

COVID-19 Impact Analysis

SARS-CoV-2, along with SARS-CoV and MERS-CoV, is the third coronavirus to emerge as a cause of severe and frequently fatal pneumonia epidemics in humans (Middle East Respiratory Syndrome-coronavirus). As with many infectious diseases, the immune response to coronavirus infection can be a double-edged sword: necessary for promoting antiviral host defense and capable of inciting life-threatening immunopathology if not properly regulated. Chemokines, a large family of leukocyte chemoattractants that coordinate leukocyte infiltration, positioning, and activation in infected tissue by acting on specific G protein-coupled receptors, are important immunoregulatory mediators. Chemokines act on G protein-coupled receptors (GPCRs), a rich target for drug development in general. The pharmaceutical industry has extensively investigated chemokine receptors with many blocking agents now in clinical trials for a variety of disease indications. The 18 known human chemokine GPCRs, like all GPCRs, have seven transmembrane domains and communicate via heterotrimeric G proteins. Local and systemic chemokine induction during many types of acute viral pneumonia has been directly correlated with disease severity in humans. Specific chemokines and chemokine receptors have been shown to play important roles in disease pathogenesis in some cases. Hence, COVID-19positively impacted theatypical chemokine receptor 3 market growth.

Atypical Chemokine Receptor 3 Market Segment Analysis

Atherosclerosis is expected to dominate the atypical chemokine receptor 3 market growth

Cardiovascular diseases (CVDs) comprise a wide range of conditions that affect the heart and blood vessels and can result in potentially fatal events such as myocardial infarction (MI), stroke, and aneurysm. Atherosclerosis, a lipid-driven, chronic inflammatory disease that affects arteries, is the primary pathology underlying CVDs. Atherosclerosis is caused by endothelial damage caused by hemodynamic shear stress, which increases endothelial permeability and, as a result, susceptibility to lipid invasion. Chemokines, also known as chemotactic cytokines, were discovered to control immune cell migration during inflammation and, later, during homeostasis. Chemokines may collaborate in the sense that some trigger integrin activation to induce firm arrest of leukocytes on activated endothelial surfaces, while others guide leukocytes to subendothelial locations via chemotaxis.

Furthermore, chemokines can influence leukocyte activation, monocyte survival, foam cell formation, smooth muscle cell (SMC) proliferation, cell egress from lesions, (lymph)angiogenesis, and thrombus formation, all of which have a significant impact on CVD. Among the various chemokines identified to alter MI3 and atherosclerosis, novel findings as well as promising therapeutic properties of the chemokines CCL5 (CC-chemokine ligand 5), CX3CL1 (CXXXC-chemokine ligand 1), CCL2, CXCR2 (CXC-chemokine receptor 2), and CXCR3, as well as the CXCL12/CXCR4 axis, have shown to have distinct roles in atherosclerosis. However, it is now clear that chemokines can modulate many other cellular functions in several immune cell populations, including proliferation, survival, differentiation, mobilization, cytokine release, and phagocytosis.  Given their immunologically relevant functions, it is not surprising that chemokines and their receptors play an important role in various stages of atherosclerosis, including leukocyte trafficking and the influx into atherosclerotic plaques, as well as cell proliferation, apoptosis, and foam cell formation within lesions. With an increasing incidence of CVD, there is increasing demand for atypical chemokine receptor 3 for atherosclerosis. For example, cardiovascular diseases (CVDs) are the leading cause of death worldwide, claiming the lives of an estimated 17.9 million people each year.

Atypical Chemokine Receptor 3 Market Geographical Share

North America region accounted for the largest market sharein the global atypical chemokine receptor market

With the increasing incidence of cardiovascular disease, this region is expected to dominate the market growth.  CVD is the leading cause of death in the United States for men, women, and people of most racial and ethnic groups. In the U.S, one person dies from cardiovascular disease every 36 seconds. Every year, approximately 659,000 people in the United States die from heart disease, accounting for one out of every four deaths.

There is an increase in systemic inflammatory activity in patients with coronary artery disease, as evidenced by an increase in the proportion of IFN-positive Th1 lymphocytes. CXCL9, CXCL10, and CXCR3 have been found to have increased systemic expression in patients with stable angina pectoris. Lower levels of these chemokines and CXCR3 were found in the peripheral cells of patients with the acute coronary syndrome, indicating a sequestering of circulating CXCR positive cells from blood to the site of infarction via intense in situ release of these chemokines. Compared to healthy controls, plasma levels of CXCL12 are lower in patients with stable and unstable angina. As a result, CXCL12 may have a protective effect in unstable angina by stabilizing the atherosclerotic plaque.

Other anti-inflammatory molecules known to protect against cardiovascular disease were discovered to influence T cell trafficking via the chemokine system. Adiponectin has been shown to inhibit the production of CXCR3 ligands in macrophages, whereas heparin competes for binding with CXCL9, CXCL10, and CXCL11 on endothelial cells. Hence, this correlation of CXCR3 with heart disease is expected to dominate the market growth in this with increasing CVD incidence.

Atypical Chemokine Receptor 3 Market Companies

The global atypical chemokine receptor 3 market is moderately competitive with a smaller number of FDA approvals and some key players.

Some of the key players in the global atypical chemokine receptor 3 market are ChemoCentryx Inc, Jyant Technologies Inc, Polyphor Ltd,X4 Pharmaceuticals, Inc., PeproTech, Inc. and OriGene Technologies, Inc.

ChemoCentryx

Overview: ChemoCentryx is a biopharmaceutical company specializing in inflammatory, autoimmune, and cancer diseases. ChemoCentryx seeks to discover, develop, and commercialize orally-administered therapies by targeting the chemokine and chemoattractant systems.

Product Portfolio: The company has many drugs in the pipeline, for example, complement inhibition for orphan diseases TAVNEOS(avacopan), Avacopan (formerly CCX168) / C5aR, in immuno-Oncology CCX559 / PD-1 / PD-L1, and for other inflammatory and autoimmune diseases CCX507 / CCR9 and CCX587 / CCR6.

Key Development: On October 8, 2021, the FDA approved TAVNEOSTM (avacopan) to treat ANCA-associated vasculitis.TAVNEOS inhibits only the C5aR, allowing the beneficial C5a pathway via the C5L2 receptor to function normally.