BDCA2

Anaptys licenses exclusive global development and commercialization rights to a potential best-in-class BDCA2 modulator portfolio IND filing to support clinical development of ANB101 in autoimmune and inflammatory diseases expected in H2 2024 Reiterating year-end 2023 cash and investments of $400 to $410 million and cash runway through year-end 2026 AnaptysBio, Inc. (Nasdaq: ANAB), a clinical-stage biotechnology company focused on delivering innovative immunology therapeutics, today announced an exclusive license agreement for Centessa Pharmaceuticals’ (NASDAQ: CNTA) blood dendritic cell antigen 2 (BDCA2) modulator antibody portfolio, including lead asset CBS004 and related family of backup antibodies, for the treatment of autoimmune and inflammatory diseases. Anaptys anticipates filing an IND application for CBS004, which will be renamed ANB101, in H2 2024. “Acquiring the rights to this BDCA2 modulator portfolio, which specifically targets plasmacytoid dendritic cells, known to be key drivers of interferon secretion and antigen presentation, complements our portfolio of best-in-class immune cell modulators to drive differentiated clinical outcomes in systemic, heterogeneous autoimmune and inflammatory diseases,” said Daniel Faga, president and chief executive officer of Anaptys. “We now plan to file two INDs in 2024: ANB101 in H2 2024 and ANB033, our CD122 antagonist, in H1 2024.” “We are pleased to enter into this agreement with Anaptys, which enables the continued advancement of Centessa’s BDCA2 modulators,” said Saurabh Saha, M.D., Ph.D., chief executive officer of Centessa. “With their focus on developing immune cell modulators, Anaptys is well positioned to further the research and development of this program in autoimmune and inflammatory diseases.” Plasmacytoid dendritic cells (pDCs) are a key upstream node in the inflammatory cascade that serve as a bridge between innate and adaptive immunity. They have been shown to be prolific secretors of type I interferons, which drive activation of a variety of downstream cell types including T cells and monocytes. Together with their ability to present antigens to the adaptive immune system, this creates a pro-inflammatory environment for the establishment and perpetuation of autoimmune pathology. BDCA2 is a molecule specifically expressed on pDCs, a class of immune cells which, while found in relatively small numbers in healthy patients, are enriched in patients with a variety of inflammatory diseases, that is critical to the regulation of toll-like receptor signaling and interferon secretion. BDCA2 has been implicated in the pathophysiology of systemic lupus erythematosus (SLE), where there exists mechanistic clinical proof of concept for pDC modulation. ANB101 is a potentially best-in-class BDCA2 modulator antibody that targets pDCs and potently inhibits interferon secretion and modulates antigen presentation for the treatment of autoimmune and inflammatory diseases. Under the terms of the agreement, Anaptys will receive from Centessa Pharmaceuticals an exclusive, global license for ANB101. Anaptys will also receive the same rights to ANB102, an extended half-life BDCA2 modulator with the potential to enable quarterly or less frequent dosing. ANB101 has successfully completed IND-enabling studies and manufacturing scale-up. Anaptys will assume responsibility for all future clinical development. In exchange, Anaptys will pay Centessa a one-time upfront cash payment of $7 million, inclusive of a one-time cash payment of $3 million for manufactured and released GMP supply of ANB101. Centessa is eligible to receive an additional development milestone payment and low single-digit royalties on global net sales. Anaptys is a clinical-stage biotechnology company focused on delivering innovative immunology therapeutics. It is developing immune cell modulators, including two checkpoint agonists for autoimmune and inflammatory disease: rosnilimab, its PD-1 agonist, in a Phase 2b trial for the treatment of rheumatoid arthritis and in a Phase 2 trial for the treatment of ulcerative colitis; and ANB032, its BTLA agonist, in a Phase 2b trial for the treatment of atopic dermatitis. Its preclinical immune cell modulator portfolio includes ANB033, an anti-CD122 antagonist antibody, and ANB101, a BDCA2 modulator antibody, for the treatment of autoimmune and inflammatory diseases. In addition, Anaptys has developed two cytokine antagonists available for out-licensing: imsidolimab, an anti-IL-36R antagonist, in Phase 3 for the treatment of generalized pustular psoriasis, or GPP, and etokimab, an anti-IL-33 antagonist for the treatment of respiratory disorders that is Phase 2/3 ready. Anaptys has also discovered multiple therapeutic antibodies licensed to GSK in a financial collaboration for immuno-oncology, including an anti-PD-1 antagonist antibody (Jemperli (dostarlimab-gxly)) and an anti-TIM-3 antagonist antibody (cobolimab, GSK4069889). To learn more, visit www.AnaptysBio.com or follow us on LinkedIn and X. The content above comes from the network. if any infringement, please contact us to modify.

Anaptys reiterated its cash runway in the statement to disclose the licensing of ANB101 Biogen has a new rival for the BDCA2 space. AnaptysBio is picking up a distant potential challenger to the big biotech’s late-phase lupus candidate, paying Centessa Pharmaceuticals $7 million upfront for rights to a preclinical prospect that is still months away from being submitted for testing in humans.  BDCA2 is expressed exclusively on plasmacytoid dendritic cells. By binding to the antigen, antibodies can suppress the production of type I interferon and, in theory, improve outcomes in patients with diseases driven by the cytokine. Biogen reported midstage data on its drug candidate, litifilimab, in systemic lupus erythematosus last year and is running a phase 3 trial in the indication. Centessa picked up its BDCA2 program from Capella BioScience, one of the 10 biotechs it rolled up when it set up shop in 2021. Capella and Centessa have shared preclinical data on their lead BDCA2 candidate, CBS004, in systemic sclerosis, also known as scleroderma. Rather than take CBS004 into the clinic, Centessa, which is dissolving Capella and other U.K. businesses, has decided to offload the program to Anaptys for $7 million upfront. The fee includes a one-time cash payment of $3 million for manufactured and released GMP supply of CBS004, now renamed ANB101.  A $10 million milestone payment, in either cash or shares, is tied to the start of the first phase 3 trial.  In a statement, Anaptys CEO Daniel Faga outlined how ANB101 fits into the biotech’s strategy, explaining that it “specifically targets plasmacytoid dendritic cells, known to be key drivers of interferon secretion and antigen presentation” and complements its “immune cell modulators to drive differentiated clinical outcomes in systemic, heterogeneous autoimmune and inflammatory diseases.” Anaptys is adding ANB101 to its list of candidates that are set to join its two lead programs in the clinic. The biotech plans to file to study its CD122 antagonist ANB033 in humans in the first half of next year. An IND filing for ANB101 is slated for the second half of 2024. The candidates will sit alongside the PD-1 agonist rosnilimab and BTLA agonist ANB032 in Anaptys’ clinical-phase pipeline. Anaptys has started phase 2b trials of both candidates, in rheumatoid arthritis, ulcerative colitis and atopic dermatitis, in recent quarters, teeing up a series of data drops spanning from the end of next year through to the first half of 2026. Anaptys reiterated its cash runway in the statement to disclose the licensing of ANB101. The biotech still expects its money to fund operations through the end of 2026, giving it a shot at generating clinical data that drives up its share price before needing to seek additional funding.

Severe Covid-19 in epithelial barrier disrupted subjects DAVOS, Switzerland , July 9, 2023 /PRNewswire/ -- According to the epithelial barrier theory, disruption of epithelial barriers by environmental and toxic agents triggers microbial dysbiosis, bacterial translocation to subepithelial areas and local or systemic immune/inflammatory response to environmental agents, allergens and microbes. Such events have been implicated in the development of chronic conditions like allergic, autoimmune, and metabolic diseases, such as diabetes, obesity, rheumatoid arthritis, allergies, asthma, atopic dermatitis. In severe cases of COVID-19, characteristic features include hyperinflammation, hyperactivated immune responses (referred to as the cytokine storm), cellular infiltration, and organ damage. Biomarkers of intact or defective epithelial barriers are associated with disease severity The compromised epithelial barriers in the mucosas, particularly in gut mucosa facilitates the translocation of microbiota and their secreted metabolites, thus initiating or exacerbating inflammatory cascades in many inflammatory diseases. The research group of epithelial biology in the Swiss Institute of Allergy and Asthma Research, associated with the University of Zurich, has been working on epithelial barriers for more than 20 years. Today they have published a study in Allergy, Journal of the European Academy of Allergy and Clinical Immunology providing substantial evidence that epithelial barrier function is compromised in particularly severe COVID-19 patients, which is also in line with the epithelial barrier theory. The authors analyzed the amount of bacterial DNA leakage to circulation and showed the link between disrupted epithelial barriers and an excessive inflammatory response. They identified other major inflammatory proteins, AREG, AXIN1, CLEC4C, CXCL10, CXCL11 and TRANCE correlated strongly with bacterial translocation and can be used to predict and discriminate severe COVID-19 cases from healthy controls and mild cases. Interestingly all of these analyses were done at the time of hospital admission even before severe symptoms occurred demonstrating that there is a link between certain protein biomarkers and disease progression from moderate to severe COVID-19 and death. These findings emphasize the value of early detection of biomarkers of epithelial barrier leakiness and bacterial translocation as indicators of poor disease outcome. They have implications on other infections, chronic diseases and may change the daily clinical practice and facilitate early therapeutic interventions. Free Access Link to the article for further reading: Correspondence: Ismail Ogulur, Cezmi A. Akdis E-mails : [email protected], [email protected] Telephone : ++41 77 258 66 84, ++41 78 738 82 84 SOURCE SIAF