On April 10, 2021 Tallac Therapeutics, Inc., a privately held biopharmaceutical company harnessing the power of innate and adaptive immunity to fight cancer, reported the first presentation of preclinical data demonstrating potent single-agent anti-tumor activity in preclinical cancer models with systemically administered TAC-001, the company’s lead clinical candidate from its novel Toll-like Receptor Agonist Antibody Conjugate (TRAAC) platform (Press release, Tallac Therapeutics, APR 10, 2021, View Source [SID1234577853]). The data will be presented today as part of the Immunomodulatory Agents and Interventions Session at Week I of the American Association of Cancer Research’s (AACR) (Free AACR Whitepaper) 2021 Virtual Annual Meeting (#AACR21) taking place April 10-15, 2021.

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Toll-like receptor (TLR) agonists are a novel class of immunotherapy that generate both an innate and adaptive immune response which may produce more robust and durable anti-cancer immunity to help overcome resistance to standard-of-care oncology treatments. TLR9 is a key intracellular TLR present in broad immune cell populations such as B lymphocytes and myeloid cells. Recent studies have shown that the likelihood of patients responding to immune checkpoint inhibitor therapy may depend on B cells in the tumor.i B cells play pivotal roles in the immune defense system, which bridge the innate and the adaptive immunities against cancers.ii In preclinical studies, the activation of TLR9 in human and mouse models drives B cell proliferation and differentiation.iii

"The results presented today at AACR (Free AACR Whitepaper) elucidate the unique properties of TAC-001 responsible for integrating B cells and TLR9 activation which trigger innate and adaptive immune responses to create potent, systemically delivered anti-tumor immunity across solid tumor types," said Dr. Hong I. Wan, president, CEO and co-founder of Tallac Therapeutics. "The emerging data on TAC-001 continues to strengthen our understanding of the roles that B cells and TLR9 activation play in eliciting anti-tumor immunity in checkpoint inhibitor resistant and refractory settings and will help guide our clinical development strategy."

In the e-poster, titled "TAC-001, a toll-like receptor 9 (TLR9) agonist antibody conjugate targeting B cells, promotes anti-tumor immunity and favorable safety profile following systemic administration in preclinical models," investigators present data providing evidence that in vitro targeted delivery of TAC-001 leads to superior TLR9 activation in B cells, increased expression of co-stimulatory molecules and cross-presentation leading to T cell proliferation. In vivo, TAC-001 demonstrated robust, curative and durable single agent anti-tumor activity in checkpoint inhibitor resistant and refractory tumor models. Additionally, the systemic administration of TAC-001 was shown to trigger both innate and adaptive immunity by increasing B cell infiltration, T effector cell functions and modulation in suppressive myeloid cells within the tumor microenvironment. These results support the development of TAC-001 for a broad range of solid tumor malignancies.

AACR Poster Presentation Details:

Title: TAC-001, a toll-like receptor 9 (TLR9) agonist antibody conjugate targeting B cells, promotes anti-tumor immunity and favorable safety profile following systemic administration in preclinical models
Session Type: E-Poster Session
Session Category: Immunology
Session Title: Immunomodulatory Agents and Interventions
Track: Immunology, Clinical Research Excluding Trials
Permanent Abstract Number: 1721
About TAC-001

TAC-001 is a Toll-like Receptor Agonist Antibody Conjugate (TRAAC) comprised of a potent Toll-like Receptor 9 agonist (T-CpG) conjugated to an anti-CD22 antibody, a receptor restricted to B cells. TAC-001 is designed to systemically deliver T-CpG to B cells by binding to CD22, leading to internalization of TAC-001, TLR9 signaling, B cell activation and a cascade of immune reactions. Preclinical studies demonstrate that the innate and adaptive immune responses triggered by TAC-001 leads to potent anti-tumor activity. TAC-001 is being developed to systemically deliver targeted immune activation in solid tumor cancers.

On April 10, 2021 Molecular Partners AG (SIX: MOLN), a clinical-stage biotech company that is developing a new class of custom-built protein drugs known as DARPin therapeutics, reported the presentation of four posters highlighting research across its immuno-oncology programs at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) virtual Annual Meeting (Press release, Molecular Partners, APR 10, 2021, View Source [SID1234577852]). The preclinical data shared include results from the Company’s acute myeloid leukemia (AML) CD3 T-cell engager program, new data from the MP0317 (FAP x CD40) tumor localized immune activator, and initial results from the Company’s CD3 prodrug programs.

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"With our new technologies designed for localized immune activation, targeting of cell surface-displayed peptides derived from intracellular proteins, and T-cell engagement, we believe we have a solid strategy for our new immune-oncology product candidates, and novel design capabilities that have the potential to greatly benefit our own and partnered immuno-oncology programs," said Daniel Steiner, Ph.D., SVP Research of Molecular Partners. "Our first T-cell engager program is focused on AML, where statistically about half of people diagnosed relapse after treatment and die from the disease. Despite the existence of approved therapies, patients are often unable to benefit from these treatments due to intolerable toxicity. We believe we have made significant progress toward finding a way to avoid this trade-off and widen the therapeutic window for T-cell engagers in AML, aiming to deliver deeper and broader anti-tumor effect and reduce the impact on patients’ healthy cells."

In preclinical studies, the Company’s AML candidates demonstrated substantial activity against different populations of AML cells in vitro, without significant damage to healthy cells. As shown in the poster titled Novel multi-specific DARPin T-cell engager with an improved therapeutic window to overcome dose limiting toxicities in AML therapies, Molecular Partners is building on the strength of the DARPin platform to create a single product designed to target three different cancer antigens simultaneously (CD70, CD33, and CD123). The multi-specific DARPin T-cell engager candidate is designed to deliver highly potent and specific activity on AML cells, with a reduced effect on healthy normal cells, and with the potential to counteract target escape mechanisms expected due to tumor heterogeneity. In an ex vivo assay using fresh blood from healthy donors, the candidate induced profoundly less inflammatory cytokine production and reduction in platelet counts, unlike simultaneously tested T-cell engager candidates in development by other parties. We believe these data support the designed capability of this candidate to kill a broader population of AML cells while decreasing risk of toxicity.

The T-cell engager research presented today also displays the Company’s prodrug DARPin technology for tumor-localized release of immune stimulation, through incorporation of a protease cleavable blocker DARPin molecule. As CD3-binding T-cell engagers are highly potent and can lead to systemic toxicities, Molecular Partners has developed a DARPin domain designed to mask the CD3 engager from interacting with T cells systemically/outside of the tumor. This technology is aimed at focusing the power of the effector function and reduce toxicities by controlling the location of activation to the tumor microenvironment. In a poster titled A solution to T-cell engager toxicity: An anti-CD3 Prodrug DARPin (CD3-PDD) shows no toxicity, but potent anti-tumor activity in a humanized mouse model, Molecular Partners presents an anti-CD3 Prodrug DARPin molecule, CD3-PDD, consisting of an EGFR-binder and a CD3-binder, linked via a protease-cleavable linker to a DARPin domain masking the CD3 effector function. This-anti EGFR x anti-CD3 – Blocker Prodrug is shown to be unable to bind and recruit T-cells in its non-cleaved state in circulation, and is designed to become activated in the tumor microenvironment upon cleavage of the linker by tumor-associated proteases.

With respect to MP0317, a multi-specific DARPin product candidate targeting both FAP and CD40 to enable tumor-localized immune activation, new preclinical data demonstrated a localized activation of immune cells in vitro, as well as ex vivo in human tumor samples, dependent on the presence of the FAP protein, which is highly expressed in the stroma of a broad range of solid tumors. The data presented in the poster titled MP0317, a FAPxCD40 targeting multi-specific DARPin therapeutic, drives immune activation and leads to macrophage repolarization in vitro and ex vivo shows that MP0317 led to macrophage repolarization and reversion of T cell suppression: MP0317 led to upregulation of CD80, an M1 marker, and downregulation of CD163, an M2 marker, only in the presence of FAP, indicating macrophage repolarization towards an M1 phenotype. Furthermore, when these repolarized macrophages were co-cultured with T cells, T cell suppression was shown to revert and CD8 T-cell activation was observed, as shown by the increase of CD25. In both assays the killing effect was comparable to that achieved by an anti-CD40 antibody. We believe these data support MP0317’s potential to deliver tumor-localized CD40-mediated immune cell activation while avoiding systemic toxicity seen in other agents. MP0317 is anticipated to begin clinical trials in the second half of 2021.

Finally, with respect to the Company’s peptide-MHC targeting program, the Company presents preclinical results from a proof of concept study targeting a peptide derived from the NY-ESO-1 protein displayed in the context of a HLA-A2 molecule (a human MHC protein). The poster, Application of the DARPin technology for specific targeting of tumor-associated MHC class I: peptide complexes, highlights results demonstrating rapid and reliable generation of DARPin proteins against pMHC which were then formatted into bispecific T-cell engagers, and engineered to enable potent and specific activation of T cells. Further, the results show that the pMHC-targeting DARPin candidate was able to achieve systemic half-life extension with limited impact on potency.

The posters presented at AACR (Free AACR Whitepaper) are available to view in the Scientific Presentations section of Molecular Partners’ corporate website.

About Molecular Partners’ Immuno-oncology Product Candidates
Molecular Partners is developing several candidates designed to activate the immune system to fight cancer while reducing damage to healthy cells. These candidates use multiple novel DARPin technologies potentially applicable against a wide range of tumor types, including DARPin candidates with the ability to restrict immune activation to the tumor microenvironment, the ability to target intracellular disease-associated proteins, and multiple novel control mechanisms for immune activation designed to direct immune attack to the right cells, at the right place, and at the right time. These capabilities can be combined during candidate design through the inherent modularity of the DARPin platform, to provide precise control over immune activation and potentially enable more effective cancer immunotherapies.

On April 10, 2021 Harpoon Therapeutics, Inc. (NASDAQ: HARP), a clinical-stage immunotherapy company developing a novel class of T cell engagers, reported the availability of three poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (Press release, Harpoon Therapeutics, APR 10, 2021, View Source [SID1234577851]). The presentations will be available beginning today at 8:30 a.m. ET through the virtual meeting website at www.aacr.org and on the Harpoon corporate website at www.harpoontx.com.

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Key findings of each of the posters are described below.

FLT3-targeting TriTACs are T cell engagers for treatment of acute myeloid leukemia
Presenter: Richard J. Austin, Ph.D., Abstract #: 2643

FLT3 RNA is found in over 95% of AML samples and FLT3 mutations are oncogenic and found in approximately 30% of AML. This provides the rationale that a FLT3-targeting T cell engager could be a valid therapeutic approach for AML. Data show that FLT3 TriTACs bind human and non-human primate FLT3, and can redirect T cells to kill FLT3 expressing cells in vitro. In addition, FLT3 TriTACs eliminate FLT3 expressing cells in a non-human primate study and are well tolerated after a single dose.

ProTriTAC is a modular and robust T cell engager prodrug platform with therapeutic index expansion observed across multiple tumor targets
Presenter: S. Jack Lin, Ph.D., Abstract #: 933

ProTriTAC is a conditionally active T cell engager platform that is designed to be preferentially active in the tumor. This enables the targeting of more broadly expressed solid tumor targets and allows T cell engagers to address more tumor types. Data presented today illustrate the consistency and the robustness of the ProTriTAC platform in vitro and in vivo as demonstrated by cell-based assays, pharmacokinetic studies in non-human primates, and therapeutic index assessments in tumor-bearing animals across multiple tumor targets. IND-enabling studies are currently underway for Harpoon’s first ProTriTAC program (HPN601).

Combinatorial antitumor effects of CD3-based trispecific T cell activating constructs (TriTACs) and checkpoint inhibitors in preclinical models
Presenter: Mary Ellen Molloy, Ph.D. Abstract #: 1573

TriTAC molecules induce PD1/PD-L1 expression on T cells which may lead to suppression of the cytolytic functions of TriTAC activated T cells. PD1 can be readily detected on T cells subsequent to the engagement of the TCR by the TriTAC molecule. Data presented today show that the combination of HPN536 with a PD-L1 inhibitor led to more potent antitumor activity in an MSLN expressing ovarian cancer xenograft model. Similar enhanced anti-tumor effects were shown in an MSLN expressing lung cancer model for HPN536 in combination with anti-PD1 or an anti-PD1 antibody. These data demonstrate the potential utility of PD1/PD-L1 blockade to enhance the potency of TriTAC mediated tumor cell killing.

"These data from Harpoon’s poster presentations at AACR (Free AACR Whitepaper) underscore the potential for further investigations of additional tumor targets, combination approaches with TriTACs, and conditionally active T cell engager prodrugs, or ProTriTACs, which may lead to greater tumor specificity, enhanced efficacy, and improved tolerability for patients," said Holger Wesche, Ph.D., chief scientific officer of Harpoon Therapeutics. "I am encouraged by these findings and look forward to future validation in the clinic."

On April 10, 2021 Blueprint Medicines Corporation (NASDAQ: BPMC) reported data from multiple poster presentations highlighting the breadth of the company’s precision therapy pipeline at the virtual American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2021 (Press release, Blueprint Medicines, APR 10, 2021, View Source [SID1234577850]). Collectively, the presentations, including foundational preclinical data for multiple programs, demonstrate the productivity of the company’s scientific platform. Additional presentations of clinical data for AYVAKIT (avapritinib) and BLU-263 will be reported on Sunday, April 11, 2021.

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"Our data presentations at the AACR (Free AACR Whitepaper) annual meeting showcase Blueprint Medicines’ next wave of precision therapies, which have the potential to impact large global patient populations," said Fouad Namouni, M.D., President, Research & Development at Blueprint Medicines. "Building on the foundation of our approved medicines AYVAKIT and GAVRETO, these presentations highlight our efforts to address significant patient needs in areas such as EGFR-driven lung cancer, cyclin E-aberrant cancers and cancer immunotherapy. As we celebrate our 10th anniversary as a company, and our rapidly expanding pipeline now includes our ninth development candidate, we look forward to continuing to leverage our productive research platform to advance potent and selective inhibitors that have the potential to enable transformative benefit for patients."

BLU-701 and BLU-945: Double- and triple-mutant inhibitors in EGFR-driven NSCLC

Lung cancer is the leading cause of cancer death globally, and approximately 17 percent of patients with lung adenocarcinoma, the most common form of non-small cell lung cancer (NSCLC), have EGFR-driven disease. While first- and third-generation EGFR inhibitors have improved treatment outcomes for patients with EGFR-driven NSCLC, resistance inevitably emerges, with the T790M and C797S mutations being the most common on-target resistance mechanisms. Together, BLU-701 and BLU-945 are designed to provide comprehensive coverage of the most common activating and on-target resistance mutations, spare wild-type EGFR to limit toxicities driven by wild-type EGFR inhibition and treat or prevent central nervous system (CNS) metastases. Ultimately, with these characteristics, BLU-701 and BLU-945 have the potential to be used either as monotherapy or in combination, together or with other agents, to potentially overcome or prevent on-target resistance across multiple lines of treatment.

BLU-701 is a potential best-in-class, selective, potent, fourth-generation double-mutant EGFR inhibitor with activity against EGFR activating mutations and the C797S osimertinib-resistant mutation. Preclinical data presented at the conference showed strong and durable inhibition of tumor growth at doses that are EGFR wild-type sparing. BLU-701 also indicated significant CNS penetration in preclinical models, with comparable exposure in the plasma and brain, which illustrates its potential to treat or prevent CNS metastases in patients with EGFR-driven tumors. With activity also shown against the activating EGFR mutants, BLU-701 has potential to be used in both first- and second-line settings.

BLU-945 is a potential first- and best-in-class, selective, potent, fourth-generation triple-mutant EGFR inhibitor with activity against the T790M and C797S resistance mutations. BLU-945 is highly selective over wild-type EGFR and off-target kinases, highlighting its potential to enable tolerable combinations with BLU-701 or other therapies. Data presented at the conference demonstrated potent anti-tumor activity in triple-mutant osimertinib-resistant tumor models, as well as activity in a triple-mutant intracranial patient-derived xenograft model. In addition, the combination of BLU-945 with either gefitinib or osimertinib showed enhanced anti-tumor activity when compared with either gefitinib or osimertinib alone.

The preclinical data presented for BLU-701 and BLU-945 support the continued development of both candidates in patients with EGFR-driven NSCLC. An investigational new drug (IND) application for BLU-945 has been cleared by the U.S. Food and Drug Administration (FDA) and an international Phase 1 dose escalation trial is expected to begin this quarter. Future clinical development of BLU-945 in combination with other agents across multiple treatment settings is planned. BLU-701 is expected to enter clinical development later this year.

BLU-222: CDK2 inhibitor in cyclin E-aberrant cancers

Cyclin dependent kinases (CDKs) and their cyclin partners regulate the cell cycle. In subsets of patients across multiple cancer types, aberrant cyclin E (CCNE) hyperactivates CDK2, resulting in cell cycle dysregulation and tumor proliferation. Aberrant CCNE has been observed as a primary driver of disease as well as a mechanism of resistance to CDK4/6 inhibitors and other therapies. In addition, data have shown that ovarian and hormone-receptor-positive breast cancer patients with aberrant CCNE have poor outcomes. Prior drug discovery efforts targeting CDK2 have been hindered by challenges in achieving selectivity over other CDK family members associated with toxicity.

At AACR (Free AACR Whitepaper), preclinical data highlighted a set of potent and selective CDK2 inhibitors designed by Blueprint Medicines. The data showed that selective CDK2 inhibition arrested the cell cycle and blocked tumor proliferation in CCNE-amplified cell lines and demonstrated robust and sustained anti-tumor activity in vivo in models of CCNE-amplified ovarian, breast and gastric cancer. A selective CDK2 inhibitor also showed improved tolerability compared to a pan-CDK inhibitor and chemotherapy, as measured by animal body weight.

Based on this work and further optimization, Blueprint Medicines reported the nomination of a potentially best-in-class selective and potent CDK2 inhibitor development candidate, BLU-222, which is expected to enter clinical development in the first half of 2022.

BLU-852: MAP4K1 inhibitor

MAP4K1 is a well-characterized immunokinase target involved in the regulation of immune cells; however, prior drug discovery efforts have been hindered by challenges in achieving selectivity over other MAP4K family members associated with toxicity. In January 2021, Blueprint Medicines announced the nomination of a highly selective and potent MAP4K1 inhibitor development candidate, BLU-852, with best-in-class potential.

Data presented at AACR (Free AACR Whitepaper) highlighted a set of potent and highly selective MAP4K1 inhibitors designed by Blueprint Medicines, including BLU-852. The inhibitors were shown to enhance intratumoral immune cell activation, overcome T cell suppression, and reduce tumor burden both as a monotherapy and in combination with checkpoint inhibition. The data support the continued development of BLU-852 under the company’s cancer immunotherapy collaboration with Roche, with Phase 1 trial initiation anticipated in 2022.

Copies of Blueprint Medicines data presentations from the AACR (Free AACR Whitepaper) annual meeting are available in the "Science—Publications and Presentations" section of the company’s website at www.BlueprintMedicines.com.

Conference Call Information

Blueprint Medicines will host a live webcast on Monday, April 12, 2021 beginning at 8:00 a.m. ET to review data for multiple research- and clinical-stage programs presented at the AACR (Free AACR Whitepaper) annual meeting. To access the live call, please dial (855) 728-4793 (domestic) or (503) 343-6666 (international) and refer to conference ID 5548976. A webcast of the conference call will be available under "Events and Presentations" in the Investors & Media section of Blueprint Medicines’ website at View Source The archived webcast will be available on Blueprint Medicines’ website approximately two hours after the conference call and will be available for 30 days following the call.

On April 10, 2021 Agenus (NASDAQ: AGEN), an immuno-oncology company with an extensive pipeline of checkpoint antibodies, cell therapies, adjuvants, and vaccines designed to activate immune response to cancers and infections, reported new clinical data on AGEN1181, its next-generation anti-CTLA-4 antibody, at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting from April 10 – 15, 2021 (Press release, Agenus, APR 10, 2021, View Source [SID1234577849]).

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"The preclinical and translational data in conjunction with our updated clinical data with AGEN1181 alone or in combination with our PD-1, balstilimab, continue to strongly support and differentiate our next-generation CTLA-4 antibody," said Steven O’Day, MD, Chief Medical Officer of Agenus. "AGEN1181 is showing activity in patients with tumors which typically do not respond to first-generation CTLA-4 and PD-1 antibodies. Equally important, the safety data continues to show no immune mediated hypophysitis, pneumonitis, or hepatitis to date. Given the efficacy and favorable safety profile, we have expanded AGEN1181 into Phase 2 in colorectal cancer patients as a first step in our efforts to expand to additional important cancer indications."

In two separate presentations at AACR (Free AACR Whitepaper), Agenus showcased the optimal performance of AGEN1181 in relevant models. In addition, as the clinical data matures, additional responses as well as a conversion from a partial response to a complete response, have been observed. The new data announced today include the following clinical responses:

New partial response in the first melanoma patient treated (monotherapy)

New conversion to complete response in ovarian cancer patient (AGEN1181 plus balstilimab)

Partial response in microsatellite stable (MSS) colorectal cancer patient (AGEN1181 plus balstilimab)

Partial response in PD-L1(-) ovarian cancer patient (AGEN1181 plus balstilimab)

Partial response in MSS colorectal cancer patient (AGEN1181 plus balstilimab)

Complete response in PD-L1(-) MSS endometrial cancer patient (monotherapy)

Complete response by PET in PD-L1(-) MSS endometrial cancer patient (AGEN1181 plus balstilimab)
Presentation Details:
E-poster presentations were made available on the conference platform on April 10 at 8:30am ET. Posters with accompanying audio will be available for viewing to meeting registrants until June 21.

Session: PO.IM02.10 – Therapeutic Antibodies, Including Engineered Antibodies
Poster title: Fc-enhanced anti-CTLA-4 antibody, AGEN1181: New mechanistic insights for potent antitumor immunity and combination potential in treatment-resistant solid tumors
Abstract number: 1878
Presenting author: Antoine Tanne, PhD

Session: PO.IM02.05 – Immune Monitoring / Clinical Correlates
Poster title: Characterization of the pharmacodynamic activity of AGEN1181, an Fc-enhanced CTLA-4 antibody, alone and in combination with the PD-1 antibody balstilimab
Abstract number: 1677
Presenting author: Irina Shapiro, PhD

In addition, Dr. Steven O’Day, Chief Medical Officer, Dr. Dhan Chand, Scientific Director, Head of Drug Discovery, and Dr. Jennifer Buell, President and COO, at Agenus, will participate in a webcast hosted by Dr. Matt Phipps of William Blair on Saturday, April 10, 2021 at 10:30 a.m. ET.

Registration for the webinar can be done in advance at View Source

A replay will be available after the call on the Events & Presentations page of the Agenus website at View Source