On November 12, 2021 Aulos Bioscience, an immuno-oncology company working to revolutionize cancer care through the development of potentially best-in-class IL-2 therapeutics, reported that preclinical data for AU-007, a computationally evolved human antibody that leverages a highly differentiated approach to harnessing the power of IL-2 to eradicate solid tumors (Press release, Aulos Bioscience, NOV 12, 2021, View Source [SID1234595470]). Data were presented in a poster presentation at the 36th Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting.

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"These positive preclinical data demonstrate the ability of AU-007 to tip the balance toward immune activation and away from immune suppression by preventing IL-2 from binding to T regulatory cells," said Aron Knickerbocker, Aulos Bioscience’s chief executive officer. "While high-dose IL-2 has shown clinical benefit, associated toxicities have limited its therapeutic use. With AU-007, we are leveraging a mechanism of action unlike any other IL-2 therapeutic in development, with the potential for lower toxicity and a sustained anti-tumor response. Supported by these data, we are continuing to advance AU-007 into a Phase 1/2 clinical trial."

AU-007 mediates human immune activation by precisely blocking an epitope on IL-2 that binds to CD25. This action redirects IL-2 to promote T effector cell expansion through binding the IL-2 receptor CD122/132 dimer while uniquely breaking the IL-2 negative feedback loop and blocking T regulatory cell (Treg) expansion, which requires activation through the CD25-containing IL-2 receptor trimer (CD25/CD122/CD132). Aulos Bioscience presented data at SITC (Free SITC Whitepaper) establishing both the specificity and activity of AU-007. In preclinical studies, AU-007 was shown to bind human IL-2 with picomolar affinity and completely inhibit its binding to CD25 while preserving binding to CD122/CD132. When evaluated for activity in mouse models of cancer, administration of AU-007 complexed with human IL-2 resulted in expansion of CD8+ T effector cells, NK cells and NKT cells in a dose-dependent manner, but had no effect on the expansion of CD4+ Tregs. Additionally, AU-007 was shown to inhibit downstream signaling of IL-2 on human CD4+ Tregs, as measured by STAT phosphorylation, in a dose-dependent manner, but did not affect IL-2 signaling on human CD8+ T effector cells, NK cells and NKT cells.

Utilizing human peripheral blood mononuclear cells (PBMCs) activated only with anti-CD3/anti-CD28 co-stimulation, AU-007, but not an isotype control antibody, inhibited the proliferation of Tregs, indicating that AU-007 can capture endogenous IL-2 and prevent the Treg cell expansion negative feedback loop. By comparison, no inhibition of CD8+ T effector cell, CD4+ T effector cell, NK cell and NKT cell proliferation was observed under the same conditions. In murine models, AU-007 also demonstrated tumor growth inhibition in multiple cancers. AU-007 has been shown to be safe and well tolerated in primate toxicology studies (data not presented).

The poster presentation is available on the Aulos Bioscience website.

About AU-007
AU-007 is a computationally evolved, human IgG1 monoclonal antibody that is highly selective to the CD25-binding portion of IL-2. With a mechanism of action unlike any other IL-2 therapeutic in development, AU-007 leverages the body’s own IL-2 to reinforce anti-tumor immune effects. This is achieved by preventing IL-2 secreted by T effector cells from binding to trimeric receptors on T regulatory cells while still allowing IL-2 to bind and expand T effector cells. This prevents the negative feedback loop caused by other IL-2-based treatments and biases the immune system toward activation over suppression. AU-007 also prevents IL-2 from binding to trimeric receptors on vasculature and pulmonary endothelium, which may significantly reduce the vascular leak syndrome and pulmonary edema associated with high-dose IL-2 therapy.

On November 12, 2021 Xencor, Inc. (NASDAQ:XNCR), a clinical-stage biopharmaceutical company developing engineered monoclonal antibodies and cytokines for the treatment of cancer and autoimmune diseases, reported the presentation of new data from multiple preclinical XmAb bispecific antibody programs and its preclinical IL-12-Fc cytokine program, XmAb662, at the 36th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) (Press release, Xencor, NOV 12, 2021, View Source [SID1234595469]).

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"XmAb bispecific Fc domains enable the rapid design and simplified development of a wide range of multi-specific antibodies and other protein structures, such as engineered cytokines. At SITC (Free SITC Whitepaper), we are presenting new data from multiple preclinical programs, including our first presentation of XmAb NK cell engagers, an exciting modality that mechanistically synergizes with our investigational engineered cytokine candidates," said John Desjarlais, Ph.D., senior vice president and chief scientific officer at Xencor. "Our preclinical programs show the power of Xencor’s platform to create exciting XmAb drug candidates that access new biologies and continually supply our clinical pipeline with differentiated molecules."

The posters will be archived under "Events & Presentations" in the Investors section of the Company’s website located at www.xencor.com.

Abstract 707, "IL12 Fc-fusions engineered for reduced potency and extended half-life exhibit strong anti-tumor activity and improved therapeutic index compared to wild-type IL12 agents"

IL-12 is a potent pro-inflammatory cytokine that promotes high levels of interferon gamma secretion from T-cells and NK cells, increasing their cytotoxicity and the immunogenicity of the tumor microenvironment by making tumor antigens more visible to the immune system. Prior clinical studies have demonstrated IL-12 has significant anti-tumor activity; however, its toxicity has limited its potential. Xencor’s IL-12 program follows the same potency reduction design strategy as the Company’s IL15-Fc fusions in oncology, where reduced potency led to improved pharmacokinetics, pharmacodynamics and safety in preclinical studies. In addition, preliminary clinical data from Xencor’s IL15-Fc program, XmAb306, showed generally good tolerability and robust and sustained immune cell expansion.

IL12-Fc fusions were engineered with reduced potency in order to improve potential tolerability, slow receptor-mediated clearance and prolong half-life in vivo, compared to native IL-12. These potency-reduced IL12-Fc fusions demonstrated significant anti-tumor activity in vivo, concurrent with activation and proliferation of CD8+ T cells and with interferon gamma production.

The addition of Xencor’s half-life extending Xtend Fc mutations further improved exposure of the molecules over time. In non-human primates, the engineered cytokines had an improved pharmacokinetic profile and therapeutic window compared to a native cytokine-Fc fusion, with superior exposure, a more gradual dose response and similar levels of cytokine production in serum.

XmAb662 was selected for further development and demonstrated significant anti-tumor activity in vivo, concurrent with increases in NK cells, T cells, serum IP10 and serum interferon gamma, which were further enhanced when combined with an anti-PD-1 antibody. The Company anticipates submitting an IND application for XmAb662 in 2022.

Abstract 698, "PDL1-targeted CD28 costimulatory bispecific antibodies enhance T cell activation in solid tumors"

T cells in the tumor microenvironment require both T cell receptor (TCR) and co-stimulatory receptor engagement to achieve full activation. CD28 is a key immune co-stimulatory receptor on T cells; however, the ligands that activate T cells through CD28 are usually not expressed on tumor cells. Targeted CD28 bispecific antibodies, a new class of T cell engager, may provide conditional co-stimulation of T cells, for example, to T cells recognizing neoantigens or in concert with CD3 T-cell engaging bispecific antibodies.

Xencor engineered PD-L1 x CD28 bispecific antibodies to provide conditional co-stimulation of T cells, activating them when bound to PD-L1+ cells. PD-L1, which is expressed on many types of tumors, suppresses anti-tumor responses by the immune system and can inhibit CD28 by engaging PD-1. A PD-L1 x CD28 bispecific antibody, therefore, may promote CD28 co-stimulation and simultaneously block CD28’s suppression by PD-1.

In vitro, the combination of the PD-L1 x CD28 and a CD3 T cell engager enhanced T cell activation and proliferation compared to the CD3 bispecific alone. PD-L1 x CD28 also enhanced the interaction between T cells and antigen presenting cells and exhibited strong CD28-dependent anti-tumor activity in mice. PD-L1 x CD28 was well tolerated in non-human primates and exhibited favorable pharmacokinetics. Modeling and preclinical data suggest a dosing schedule consistent with typical checkpoint inhibitor regimens.

Abstract 872, "PD1 x TGFβR2 and CD5 x TGFβR2 bispecifics selectively block TGFβR2 on target-positive T cells, promote T cell activation, and elicit an anti-tumor response in solid tumors"

TGFβ is an inhibitory cytokine, and its production in solid tumors is a significant mechanism used by tumors to avoid recognition by the immune system. While TGFβ inhibition is expected to promote an anti-tumor response, systemic blockade of TGFβ has also been associated with toxicity.

Xencor engineered two XmAb bispecific antibodies, PD-1 x TGFβR2 and CD5 x TGFβR2, to selectively block the suppressive activity of TGFβ on specific T-cell populations and to enhance their anti-tumor activity while avoiding the toxicity associated with systemic blockade. PD-1 and CD5 were selected to direct TGFβ blockade to activated or all T cells, respectively.

In vitro, both bispecific antibodies exhibited highly selective blocking of TGFβ activity in PD-1-high and CD5-positive T cell populations. PD-1 x TGFβR2 and CD5 x TGFβR2 were active in vivo and promoted T cell engraftment and anti-tumor response. Anti-tumor activity was significantly enhanced when combined with an anti-PD-1 antibody, compared to either anti-PD-1 or the bispecific antibody alone.

Abstract 787, "Natural killer cell engagers activate innate and adaptive immunity and show synergy with proinflammatory cytokines"

Xencor’s XmAb natural killer cell engagers (NKEs) are multifunctional antibodies that target multiple activating receptors on the surface of NK cells and bind to tumor associated antigens.

Xencor engineered a B7-H3 x NKG2D NKE bispecific antibody with a modified Fc domain to enhance FcγR binding. The molecule’s design is intended to engage NK cells through the simultaneous binding to B7-H3 on tumor cells and the activating receptors NKG2D and CD16. Additionally, NKEs may provide co-stimulation to T cells through NKG2D expressed on T cells.

In vitro, B7-H3 x NKG2D NKEs activated NK cells, enhanced NK cell mediated lysis of tumor cells and provided co-stimulation to T cells. Additionally, in vitro anti-tumor activity was enhanced when combined with proinflammatory cytokines: an analog of the IL15-Fc cytokine XmAb306 and the IL12-Fc cytokine XmAb662.

On November 12, 2021 Xencor, Inc. (NASDAQ:XNCR), a clinical-stage biopharmaceutical company developing engineered monoclonal antibodies and cytokines for the treatment of cancer and autoimmune diseases, reported data from its Phase 1 study evaluating vudalimab (XmAb717), a PD-1 x CTLA-4 bispecific antibody, in patients with advanced solid tumors (DUET-2) (Press release, Xencor, NOV 12, 2021, View Source [SID1234595468]). The updated results, predominantly from the study’s expansion cohorts, are presented in a poster titled, "Preliminary clinical experience with XmAb20717, a PD-1 x CTLA-4 bispecific antibody, in patients with advanced solid tumors" at the 36th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper).

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"Data from early-stage studies suggest that PD-1 and CTLA-4 inhibition has promise in prostate cancer, an area with high unmet need and without much checkpoint use. Dual targeting of these checkpoints through a bispecific antibody with a differentiated tolerability profile could meet an important unmet clinical need. In our Phase 1 study, we have observed vudalimab to be generally well tolerated, with lower rates of some types of immunotherapy-related adverse events, and to have encouraging clinical activity," said Allen Yang, M.D., Ph.D., senior vice president and chief medical officer at Xencor. "We are now enrolling a Phase 2 study of vudalimab for patients with metastatic castration-resistant prostate cancer, as a monotherapy or in combination, depending on molecular subtype. In addition, we are initiating a second Phase 2 study in patients with advanced pelvic tumors, including clinically defined high risk mCRPC and certain gynecologic malignancies, which represent another opportunity for vudalimab’s dual targeting of PD-1 and CTLA-4 to address an unmet need."

At the data cut off, 110 patients had been treated at the 10 mg/kg recommended dose level in dose-escalation (n=7) and in five dose expansion cohorts: melanoma (n=20), renal cell carcinoma (RCC, n=21), non-small cell lung cancer (NSCLC, n=20), castration-resistant prostate cancer (CRPC, n=21) and other cancers without approved checkpoint therapies (n=21). 10 mg/kg was identified as the recommended dose for the multi-cohort, parallel-group expansion phase, based on an observation of consistent proliferation of both CD8+ and CD4+ T cells, indicative of dual checkpoint blockade, and a complete response (CR) in one patient with melanoma.

The safety analysis includes all 110 patients, who were a median of 65 years old and were heavily pretreated, having a median of four prior systemic therapies. 65% of patients had received at least one prior checkpoint therapy, and 25% had received at least two prior checkpoint therapies.

Vudalimab was generally well-tolerated, and the most common treatment-related adverse events were immune-related adverse events (irAEs). The most common irAEs of any grade were rash (45.5%), pruritus (30.9%), transaminase increases (23.6%), diarrhea (11.8%), hypothyroidism (9.1%), infusion related reaction (8.2%) and myalgia (8.2%).
As previously reported, immune-mediated pancreatitis (Grade 5) was reported for one patient with RCC, whose cancer had already metastasized to the pancreas at baseline and progressed on study, and Grade 5 myocarditis and respiratory failure were reported for a patient with NSCLC who had a history of significant cardiac events, including atrial fibrillation and the insertion of a dual-chamber pacemaker.
The efficacy analysis included 78 evaluable patients receiving any amount of vudalimab, who had been followed for at least two cycles prior to data cut.

A complete response was observed in a patient with BRCA1+ high-grade serous ovarian cancer, who had received multiple prior treatments, including olaparib and nivolumab in the metastatic setting. The patient had a partial response after Cycle 4, and by Cycle 18 of treatment all lesions had resolved except a lesion in the abdominal wall, which later showed no cancer cells upon biopsy.
A confirmed complete response was observed in a patient with melanoma during dose-escalation at the 10 mg/kg dose level, as previously reported.
Partial responses were observed in patients with melanoma (n=2), RCC (n=3), NSCLC (n=2) and CRPC (n=2). The objective response rate across cohorts was 14.1% (11/78). All responses in patients with melanoma and CRPC and two responses in patients with RCC were confirmed. All responders, except those with CRPC, had received prior checkpoint inhibitor therapy.

Of the 12 efficacy-evaluable patients with CRPC, four had measurable disease and follow-up RECIST assessments, including the two CRPC responders.
Six additional patients with CRPC, but without measurable disease, experienced a best overall response of non-CR/non-PD, as stable disease cannot be determined without measurable disease.
The two CRPC responders had visceral and nodal metastases, had response durations of 41.3 and 27.0 weeks, were without progression on bone scans and had confirmed prostate-specific antigen (PSA) reductions of more than 50% from baseline. Among twelve patients with baseline and follow-up PSA assessments, including the two responders, 33% (4/12) had PSA reductions greater than 50%.
The median duration of response, unadjusted, for all responders was 18.3 weeks. The median duration of response, unadjusted, for patients with RCC was 24.1 weeks, and two patients remained on treatment.

Pharmacodynamic analysis indicated that activation and proliferation of both CD8+ cytotoxic T cells and CD4+ helper T cells was observed, which is consistent with dual PD-1 and CTLA-4 checkpoint inhibition. Baseline serum levels of the cytokines IL-6, IL-8 and IL-10 trended lower in patients who achieved a response on study. Low baseline tumor expression of myeloid recruitment genes (CXCL3 and CXCL8) was also associated with clinical benefit.

The poster will be archived under "Events & Presentations" in the Investors section of the Company’s website located at www.xencor.com.

About Vudalimab (XmAb717)

Vudalimab (XmAb717) is an XmAb bispecific antibody that simultaneously targets immune checkpoint receptors PD-1 and CTLA-4 and is designed to promote tumor-selective T-cell activation. Xencor’s approach to dual checkpoint/co-stimulation reduces the need for the multiple antibodies and allows for more selective targeting of T cells with high checkpoint expression, which may potentially improve the therapeutic index of combination immunotherapies. In preclinical studies, dual blockade of PD-1 and CTLA-4 with vudalimab significantly enhanced T cell proliferation and activation, and anti-tumor activity in vivo. Xencor has initiated a Phase 2 clinical study of vudalimab in patients with metastatic castration resistant prostate cancer (mCRPC), as a monotherapy or in combination depending on subtype, and a Phase 2 clinical study in patients with advanced gynecologic and genitourinary malignancies, as well as clinically defined high-risk mCRPC.

On November 12, 2021 Biodesix, Inc. (Nasdaq: BDSX), a leading data-driven diagnostic solutions company with a focus in lung disease, reported that the company will co-present with Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY), three posters at the 36th Annual Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Nov. 10 – 14, 2021 from research into diagnostic tests of treatment response of NSCLC patients to immune checkpoint inhibitor therapy (Press release, Biodesix, NOV 12, 2021, View Source [SID1234595467]).

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"Biodesix is committed to performing research with biopharma companies, while pursuing, discovering and developing applications that can help physicians and researchers address the needs of patients with lung cancer who will benefit from quick, actionable test results," said Scott Hutton, CEO, Biodesix. "We are pleased to present data on two tests that have the potential to become instrumental in the care of patients with non-small cell lung cancer (NSCLC). Additionally, our data highlights novel methods that we have developed to provide an explanation as to how our proprietary Diagnostic Cortex Artificial Intelligence (AI) platform combines molecular attributes to produce individual patient results. This data is extremely important because we expect that this will provide clarity and transparency to how our AI-based tests work and how a diagnostic test may better predict efficacy of various treatments in the most appropriate patient populations. We are proud of the data being presented at SITC (Free SITC Whitepaper) as it underscores our commitment to the lung cancer community."

The three Genentech/Biodesix-sponsored posters include the following:

Abstract #26: Validation of the Primary Immune Response (PIR) test in advanced non-small cell lung cancer (NSCLC): blinded retrospective analyses from the POPLAR and OAK trials

Findings will be presented from blinded, retrospective analyses of two Genentech multicenter, open-label RCT clinical studies comparing atezolizumab versus docetaxel in patients with previously treated NSCLC (POPLAR Phase 2 and OAK Phase 3). The Biodesix liquid-biopsy mass spectrometry-based Primary Immune Response (PIR) test stratified outcomes for patients treated with the study drug in second and third line, predicting overall survival, even when adjusted for PD-L1 expression and clinical factors. The importance of understanding who will or will not respond to immunotherapy is critical and identifying predictive biomarkers of immunotherapy response has become a growing focus of immune-oncology research. This study highlights the potential of biomarkers of immune checkpoint inhibitors, such as the PIR test, to support patient stratification.

Abstract #28: Predictions of outcomes and benefit of immune checkpoint inhibitor treatment in non-small cell lung cancer require information on both tumor and host biology

Findings from a Genentech blinded, retrospective study of second- and third-line NSCLC patients in the OAK Phase 3 clinical study comparing atezolizumab versus docetaxel in patients with previously treated NSCLC will be presented. The study demonstrated that the Biodesix Anti-PD-L1 Response Test (ART), based on mass spectrometry of pretreatment serum, stratifies outcomes in both treatment arms overall and in all PD-L1 subgroups. The Biodesix ART test was shown in independent validation to predict outcomes for NSCLC patients treated in a large Phase 3 study and was discovered and developed for Genentech as a part of a partnership between the two companies.

Abstract #831: Exact Shapley Values for explaining complex machine learning based molecular tests of checkpoint inhibitors: potential utility for patients, physicians, and translational research

Data will show how Exact Shapley Values (SVs), a technique developed by Biodesix, can explain how complex machine learning (ML)-based tests combine molecular attributes to produce individual patient results. Exact SVs can be obtained for certain ML architectures used in molecular test development, revealing the overall relative importance of attributes used in such molecular tests. Specifically, this study evaluated SVs for the Biodesix Anti-PD-L1 Response Test (ART), that was shown in independent validation to predict outcomes for NSCLC patients treated in a large Phase 3 study. By subgrouping patients according to ART results, different patterns of SVs were determined, potentially revealing different biologies that were predictive of overall survival outcomes. Exact SVs explain how complex ML-based tests combine molecular attributes to produce individual patient results.

On November 12, 2021 CERo Therapeutics, Inc., a biopharmaceutical company pioneering the development of novel autologous engineered immune cell therapies, reported the results from preclinical in vitro studies describing the characterization of novel chimeric engulfment receptor (CER) T cells (Press release, Cero Therapeutics, NOV 12, 2021, View Source [SID1234595466]). CERs are genetically engineered proteins that bind to tumor-agnostic, inducible stress ligands on the surface of tumor cells to provoke tumor-specific cytotoxicity and innate immune functions such as engulfment and antigen presentation. The data, which are being presented at the 36th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) (SITC 2021), demonstrate that T cells engineered to express CERs exhibit multifunctional properties of both innate and adaptive immune responses and suggest the potential for CER T cells to overcome barriers associated with existing adoptive cell-based therapies.

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"These studies highlight for the first time the unique orthogonal profile of CER T cells to combine the tumor cell clearance attributes of macrophages and dendritic cells of the innate immune system with the T-cell activation of the adoptive immune system into a single engineered T cell," said Daniel Corey, MD, founder and CEO of CERo. "One of the limitations of activated T cells is their poor ability to present antigens due to inefficient antigen capture. In contrast, CER T cells facilitate antigen capture, processing and presentation, and impart target-dependent cytokine function, thereby offering a possible means of improving the therapeutic potential of engineered cell therapies."

In the studies, CER T cell constructs containing an extracellular phagocytic receptor were characterized for multiple functions, including cytotoxicity in combination with a Bruton’s tyrosine kinase inhibitor (BTKi), tumor cell fragment uptake, T-cell activation, cytokine induction, and antigen-presenting cell (APC)-like activity. Results of these in vitro studies showed that CER T cells synergized with a BTKi to enhance killing of a mantle cell lymphoma tumor cell line. Further, CER T cells exhibited abilities to capture tumor cell fragments and induce expression of T-cell activation markers and cytokines. CER T cells containing a toll-like receptor (TLR) domain also showed enhanced ability to present exogenous antigen and activate antigen-specific TCR T cells.

The poster entitled "Enhanced antigen capture, antigen-presenting cell (APC)-like function, and cytotoxic responses with chimeric engulfment receptor (CER) T cells" (Abstract #207) is now accessible virtually via the SITC (Free SITC Whitepaper) website and in person today from 7:00 a.m. – 8:30 p.m. ET in Exhibit Hall E.

About CERo’s Platform Technology

CERo’s technology aims to expand the therapeutic potential of engineered T cell-based therapies by introducing distinct and complementary tumor cell clearance pathways into a single T cell. By engineering T cells to express CERs, CERo’s platform technology enables T cells to target tumors, induce cellular damage, engulf tumor fragments, and clear tumors, effectively harnessing the anti-tumor attributes of both innate and adaptive immune responses. CER T-cell products are designed to generate a more complete and durable anti-tumor response. This novel biology amends itself to combinations with classic CAR T-cell or small molecule therapy and has potential applications in hematologic malignancies and solid tumors.