CD39 x TGF-β

Oral presentation highlights the resolving of inflammation and superior homing to bone marrow of CXCR4-enriched T regulatory cells. Poster presentation includes safety and efficacy data from phase 1b LIMBER-TREG108 study evaluating CK0804, CXCR4 enriched, T regulatory cells, as an add on therapy to ruxolitinib in patients with myelofibrosis who experience a suboptimal response to ruxolitinib. HOUSTON, Nov. 6, 2023 /PRNewswire/ -- Cellenkos® Inc., a clinical stage biotechnology company focused on developing allogeneic, off-the-shelf, T regulatory (Treg) cell therapies for treatment of rare inflammatory diseases and autoimmune disorders, today announces an oral presentation and poster presentation at the 65th American Society of Hematology (ASH) Annual Meeting & Exposition, which is being held December 9-12, 2023, in San Diego, California. The oral presentation will describe the differentiation and characterization of the CXCR4 enriched Treg cells and their preferential homing to bone marrow to resolve inflammation and decrease TGFβ1 and TGFβ2, in vivo, when compared to control Treg cells. This presentation has also been selected for ASH Abstract Achievement Award. The poster presentation will elaborate on the results of Company's CK0804 Phase 1b trial. The study provides first-in-human safety of multiple infusions of CK0804 in myelofibrosis patients in the ambulatory setting as well as improvement in their blood transfusion requirements and symptom burden. "We are very pleased with the breadth of our oral and poster presentations at this year's ASH meeting, which reflect the promising potential of CK0804 as the backbone for treating myelofibrosis," stated Tara Sadeghi, Chief Operating Officer of Cellenkos® Inc. "Of particular note is the convergence of our CK0804 clinical data with the strong pre-clinical hypothesis and its mechanism of action. This marks dawn of a new era of differentiated Treg cell therapy that could be tailored to specific target tissue and can be investigated in combination with existing approved therapies, especially if there are complimentary mechanisms of action and favorable side effect profiles. The ability to administer CK0804 cells in ambulatory setting without requiring lymphodepletion or hospital admission, embarks the democratization of cellular therapies such that these potentially lifesaving treatments could be made available to patients in the community setting. In addition, the improvement in blood transfusions burden allows for CK0804 to be positioned as a potential novel therapy. We look forward to examining CK0804 in a larger trial." Further details of the presentations are provided below. Oral Presentation Title: CXCR4 Enriched T Regulatory Cells Preferentially Home to Bone Marrow and Decrease Inflammation Date: Saturday, December 9, 2023. Time: 4:30 PM Location: San Diego Convention Center, Room 6A This oral presentation describes the CXCR4 enrichment of Treg cells using the CRANE™ technology platform and faster migration of CXCR4 enriched cells towards SDF1a as early as 15-minute time point. In vivo, the CXCR4 enriched Tregs preferentially trafficked to bone marrow and exhibit higher expression of CXCL12, CD62L, CD39, CD73 and CXCR5. A decrease in TGFα, TNFβ, IL-13 as well as TGFβ1 and TGFβ2 was also observed. These CXCR4 enriched Treg cells are being examined in phase 1b clinical trial (NCT05423691). Poster presentation Title: A Phase Ib, Open-Label Study of Add on Therapy with CK0804 in Participants with Myelofibrosis and Suboptimal Response to Ruxolitinib Date: Saturday, December 9, 2023 Time: 5:30 PM Location: San Diego Convention Center, Halls G-H This presentation describes the safety and efficacy data from the ongoing phase 1b LIMBER-TREG108 study evaluating CK0804, CXCR4 enriched, T regulatory cells, as an add on therapy to ruxolitinib in patients with myelofibrosis who experience a suboptimal response to ruxolitinib. This is a single arm study where patients receive 6 infusions of CK0804 at a fixed dose at 100 million Treg cells every 28 days. Clinical data from 5 patients who have completed treatment show early promising results of improvement in blood transfusion as well as relief from symptom burden. Additionally, patients report improvement in their tolerance of anemia and daily activities of life. About Cellenkos®, Inc. Cellenkos® is a clinical-stage biotechnology company located in Houston, Texas, USA, founded in 2016 with the licensing of a proprietary umbilical cord blood T-Regulatory cell therapy platform from The University of Texas at MD Anderson Cancer Center. Being derived from umbilical cord blood, Cellenkos' T-Regulatory cells are naïve, bonafide suppressor cells that resolve inflammation through multiple direct and indirect interactions. Cellenkos is dedicated to the development and commercialization of the allogeneic, off-the-shelf cell-based products for the treatment of rare inflammatory diseases and autoimmune disorders. For more information, please visit . Disclosure MD Anderson has an institutional conflict of interest with Cellenkos® related to this research and has implemented an Institutional Conflict of Interest Management and Monitoring Plan Contact: Stacy Minor [email protected] SOURCE Cellenkos, Inc.

SHANGHAI & SUZHOU, China & GERMANTOWN, Md.--(BUSINESS WIRE)-- Elpiscience Biopharmaceuticals, Inc. (“Elpiscience”), a clinical-stage biopharmaceutical company focused on developing next-generation immunotherapies to benefit cancer patients worldwide, presented studies for its innovative immunotherapeutic molecules at the SITC 2023 Annual Meeting, including KG2A/NKG2C dual-targeting antibody ES015-2, a high affinity LILRB1 specific blocking antibody ES008-a, and the first-in-class anti-CD39/TGF-βRII bifunctional fusion protein ES014. Study Highlights: Title: Selective delivery of TGFβ “trap” to CD39-expressing immune and stroma cells reshapes tumor microenvironment and rejuvenates antitumor immunity Abstract Number: 453 CD39-Adenosine and TGFβ are two key immune suppressive pathways within the tumor microenvironment (TME). TGFβ, in contrast to its biphasic effects on tumor cells, acts on stromal cells and immune cells in the TME, which commonly express high levels of CD39, to promote tumor progression. CD39-targeted TGFβ “trap” is thus more likely to effectively inhibit tumor progression. Our study showed that ES014, a bifunctional antibody–ligand trap which comprises an antibody targeting CD39 fused to a TGFβ receptor II ectodomain, can inhibit TGFβ activity and lead to cancer killing in ex vivo models. A phase I clinical study is ongoing to primarily investigate the safety, tolerability, and preliminary clinical activity of ES014 in patients with advanced solid tumors. Highlights: ES014 binds and neutralizes both CD39 and TGFβ. ES014 promoted killing of tumors from NSCLC patients in ex vivo MPE model. ES014 inhibits Treg differentiation and TGFβ-induced CD39 expression on T cells. ES014 promotes T cell survival. Title: ES015-2, a first-in-class NKG2A and NKG2C dual-targeting antibody, demonstrated potent anti-tumor immune response Abstract Number: 498 The inhibitory receptor NKG2A and the activating receptor NKG2C modulate the function of NK and CD8 T cells by recognizing the same ligand HLA-E. NKG2A is selectively expressed on lymphocytes with cytolytic function, and the NKG2C “engager” has the potential to generate a strong antitumor response against various tumors. Inhibiting NKG2A and HLA-E alone was not as effective as had been expected in both mouse tumor models and in clinical trials. Our NKG2A/NKG2C dual targeting antibody ES015-2 can inhibit NKG2A function yet promoting NKG2C action, leading to superior anti-tumor response. Highlights: ES015-2 is a NKG2A/NKG2C dual targeting antibody. ES015-2 can completely block the interaction of NKG2A/CD94 with HLA-E, thereby inhibits HLA-E-induced NKG2A inhibitory signaling. Ligation of ES015-2 effectively potentiates the activation of NKG2C+ NK cells and T cells. Title: ES008-a, a high affinity LILRB1 specific blocking antibody activates multiple immune cells to fight cancers Abstract Number: 510 LILRB1 is the most broadly expressed member of LILRB family on various immune cells. Blocking LILRB1 augments macrophage phagocytosis of tumor cells, restores cytotoxic function of NK cells, and enhances tumor cell killing by effector CD8+ T cells. The high affinity LILRB1 specific blocking antibody ES008-a can activate multiple immune cells to fight cancers. Highlights: ES008-a is a high affinity LILRB1-specific blocker that can completely block HLA-G/LILRB1 and HLA-A2/LILRB1 interactions. ES008-a promotes NK cell-mediated destruction of tumor cells. ES008-a synergizes with CD47/SIRPα inhibitors in enhancing macrophage phagocytosis of tumor cells. About Elpiscience Elpiscience is a clinical-stage biopharmaceutical company dedicated to developing life-changing immuno-oncology therapies for cancer patients worldwide. The company’s innovative approach is focused on removing immunosuppressive factors in the tumor microenvironment, by targeting the adenosine pathway and myeloid checkpoints. A pipeline of novel molecules has been developed using its proprietary platforms including a powerful Bispecific Macrophage Engager (BiME®) technology that connects and activates macrophages for solid tumor killing without causing cytokine storms. For more information, please visit: View source version on businesswire.com: Contacts BD inquiries: BD@elpiscience.com Media inquiries: PR@elpiscience.com Source: Elpiscience Biopharmaceuticals, Inc. View this news release online at:

SHANGHAI & SUZHOU, China & GERMANTOWN, Md.--(BUSINESS WIRE)-- Elpiscience Biopharma, Inc. (“Elpiscience”), a clinical-stage biopharmaceutical company focused on developing next-generation immunotherapies to benefit cancer patients worldwide, today announced it will have three poster presentations at the SITC 2023 Annual Meeting taking place November 3-5, 2023, in San Diego. The posters will highlight its studies on three innovative molecules including a first-in-class NKG2A/NKG2C dual-targeting antibody ES015, a high affinity LILRB1 specific blocking antibody ES008-a, and the first-in-class anti-CD39/TGF-βRII bifunctional fusion protein ES014 which has been proven to be able to deliver TGFβ “trap” to CD39-expressing immune and stroma cells to reshape tumor microenvironment and rejuvenates antitumor immunity. Poster presentation details: Title: Selective delivery of TGFβ “trap” to CD39-expressing immune and stroma cells reshapes tumor microenvironment and rejuvenates antitumor immunity Abstract Number: 453 Date and time: November 3, 2023; 9 am –7 pm PDT Location: Exhibit Halls A and B1 – San Diego Convention Center Title: ES015, a first-in-class NKG2A and NKG2C dual-targeting antibody, demonstrated potent anti-tumor immune response Abstract Number: 498 Date and time: November 4, 2023; 9 am –8:30 pm PDT Location: Exhibit Halls A and B1 – San Diego Convention Center Title: ES008-a, a high affinity LILRB1 specific blocking antibody activates multiple immune cells to fight cancers Abstract Number: 510 Date and time: November 4, 2023; 9 am –8:30 pm PDT Location: Exhibit Halls A and B1 – San Diego Convention Center About Elpiscience Elpiscience is a clinical-stage biopharmaceutical company dedicated to developing life-changing immuno-oncology therapies for cancer patients worldwide. The company’s innovative approach is focused on removing immunosuppressive factors in the tumor microenvironment, by targeting the adenosine pathway and myeloid checkpoints. A pipeline of novel molecules has been developed using its proprietary platforms including a powerful Bispecific Macrophage Engager (BiME®) technology that connects and activates macrophages for solid tumor killing without causing cytokine storms. For more information, please visit: