On June 2, 2022 Affini-T Therapeutics, Inc., a biotechnology company unlocking the power of T cells against oncogenic driver mutations, reported that the clinical strategy for enhancing the efficacy of its Merkel cell polyomavirus (MCPyV)-specific T cell receptor (TCR) program for the treatment of PD-1 refractory Merkel cell carcinoma (MCC), from its strategic collaboration with Fred Hutchinson Cancer Center, will be presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting 2022 (Press release, Affini-T Therapeutics, JUN 2, 2022, View Source [SID1234615468]). The poster presentation will be delivered by Joshua Veatch, M.D., Ph.D., from Fred Hutch.

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"We recognize that MCC patients are in desperate need of new treatments, in particular due to having no curative therapeutic options and a five-year survival rate of less than ten percent in those who have developed widespread disease," said Loïc Vincent, Ph.D., Chief Scientific Officer of Affini-T. "The clinical strategy to be presented at ASCO (Free ASCO Whitepaper) is the result of tumor biopsy analyses generated from treating MCC patients and reflects the recent addition of an MHC-I boosting molecule to the MCPyV-specific T cell Phase I/II study protocol. By enhancing MHC-I expression on MCC tumors, we hope to minimize immune system evasion and maximize the clinical efficacy of MCPyV-specific T cells to treat MCC patients."

Poster presentation details are as follows:

Title: ATTAC-MCC: Phase I/II study of Autologous CD8+ and CD4+ Transgenic T cells expressing a high-affinity MCPyV-specific TCR combined with checkpoint inhibitors and Class I MHC-upregulation in patients with metastatic MCC refractory to PD-1 axis blockade
Presenting Author: Joshua Veatch, M.D., Ph.D., Fred Hutchinson Cancer Center
Abstract Number: TPS9596
Poster Number: 186b
Poster Session Title: Melanoma/Skin Cancers
Date & Time: June 6, 2022, 2:15 PM EDT

About Merkel Cell Carcinoma and Merkel Cell Polyomavirus
Merkel cell carcinoma (MCC) is a highly aggressive skin cancer, with an incidence that has doubled in the last 20 years to approximately 3,000 cases per year in the U.S. Over one-third of patients will develop widespread disease and outcomes for these patients have been historically poor with a five-year survival rate of less than ten percent. Cancer-causing Merkel cell polyomavirus (MCPyV) is expressed in most MCC tumors and can be leveraged to target these tumors. Although immune checkpoint inhibitors (ICIs) targeting relevant biochemical pathways show promise, most MCC patients will eventually relapse. There is no standard of care for patients whose cancer has become resistant to ICIs. We believe that cellular immune therapies targeting MCPyV may provide additional clinical benefit to these patients.

On June 2, 2022 Emergent BioSolutions Inc. (NYSE: EBS) reported that members of the company’s executive management team will participate in the following investor conferences (Press release, Emergent BioSolutions, JUN 2, 2022, View Source [SID1234615487]):

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Benchmark Healthcare House Call Virtual 1X1 Conference
June 2, 2022
NYSE Healthcare & Technology Virtual Investor Access Day
June 8, 2022
East Coast IDEAS Conference
June 22, 2022
Pre-recorded presentation will be accessible beginning at 6:00 am ET
View Source
For conferences where a presentation is planned, the company’s webcast presentation may include a discussion of the company’s recent business developments as well as its financial results and guidance. The webcasts will be available both live, if possible, and by replay, and will be accessible from the Emergent website.

On June 2, 2022 Erasca, Inc. (Nasdaq: ERAS), a clinical-stage precision oncology company singularly focused on discovering, developing, and commercializing therapies for patients with RAS/MAPK pathway-driven cancers, reported a trial to investigate the ERK1/2 inhibitor ERAS-007 in combination with a KRAS G12C inhibitor in KRAS G12C-driven non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) (Press release, Erasca, JUN 2, 2022, View Source [SID1234639378]).

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"We look forward to ERAS-007 being evaluated in this trial, based in part on ERAS-007’s ability in preclinical studies to robustly shut down oncogenic signaling," said Jonathan E. Lim, M.D., Erasca’s chairman, CEO, and co-founder. "This trial not only helps to broaden the therapeutic development of ERAS-007, but also complements the patient subgroups within our ongoing HERKULES-2 and HERKULES-3 master protocols. Additionally, it may provide proof-of-concept data supporting the addition of ERAS-007 as a treatment option to overcome RAS/MAPK resistance with KRAS G12C inhibitors. We look forward to potentially partnering with the team to explore the therapeutic potential of this combination."

Ryan Corcoran, M.D., Ph.D., Director of the Gastrointestinal Cancer Center Program at Massachusetts General Hospital and Associate Professor of Medicine at Harvard Medical School, added, "While adaptive feedback mechanisms can overwhelm MEK inhibitors, ERK inhibitors potentially can overcome drug resistance mechanisms that involve reactivation of RAS/MAPK pathway signaling. We look forward to evaluating whether the ERK1/2 inhibitor ERAS-007 has the potential to overcome feedback mechanisms and help address the limited efficacy of single agent KRAS G12C inhibitors."

A Phase 1b clinical proof-of-concept trial will evaluate ERAS-007 in combination with a KRAS G12C inhibitor in patients with NSCLC and CRC harboring a KRAS G12C mutation. Additional preclinical and clinical laboratory research will be conducted to further understand the activity and safety of this combination in these patient populations. The trial will be led by principal investigators Scott Kopetz, M.D., Ph.D., Professor of Gastrointestinal Medical Oncology at The University of Texas MD Anderson Cancer Center, Dr. Corcoran, and Pasi Janne, M.D., Ph.D., Professor of Medicine at Harvard Medical School. Drs. Corcoran and Kopetz recently received a grant from Stand Up To Cancer (SU2C).

About ERAS-007
ERAS-007 is a potential best-in-class ERK1/2 inhibitor being investigated alone or in combination with different inhibitors targeting upstream nodes of the MAPK pathway as part of Erasca’s MAPKlamp strategy. The extracellular signal-regulated kinases (ERK), ERK1 and ERK2, belong to a family of serine-threonine kinases that regulate cellular signaling and comprise the terminal node of the RAS/MAPK pathway. The broad therapeutic potential of ERAS-007 is being investigated initially across four HERKULES clinical trials that span multiple tumor types and include both monotherapy and combinations with approved and investigational agents, such as RTK, SHP2, RAS, RAF, and/or cell cycle inhibitors. HERKULES-1 is a Phase 1b/2 clinical trial for ERAS-007 as a single agent and in combination with the SHP2 inhibitor ERAS-601 in advanced solid tumors. HERKULES-2 is a Phase 1b/2 clinical trial for ERAS-007 in combination with various agents in patients with non-small cell lung cancer. HERKULES-3 is a Phase 1b/2 clinical trial for ERAS-007 in combination with various agents in patients with gastrointestinal cancers. HERKULES-4 is a Phase 1b/2 clinical trial for ERAS-007 in combination with various agents in patients with hematologic malignancies.

On June 2, 2022 Proxygen, a leader in the discovery and development of molecular glue degraders, reported that the company has entered into a strategic multi-year research collaboration and license agreement with Merck (Press release, Proxygen, JUN 2, 2022, View Source [SID1234615419]). Proxygen is eligible to receive up to €495 million ($554 million at the average USD/EUR FX rate of Q1 2022) in continuous R&D funding, upfront and success-based pre-clinical, clinical, regulatory, and commercial milestones, as well as additional royalty payments. Under the terms of the agreement, the companies will jointly identify and develop molecular glue degraders up to a clinical candidate stage.

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"We are incredibly excited to start this long-term collaboration with Merck, a globally recognized player in the pharmaceutical industry that shares our drive towards dynamic innovation for the benefit of patients. The partnership validates the unique potential of Proxygen’s glue degrader platform and strategically leverages our common strengths in the targeted protein degradation field", says Dr. Bernd Boidol, CEO of Proxygen.

Molecular glue degraders re-direct the cell’s own quality control machinery towards disease-causing proteins, inducing their selective and complete elimination. Because of their capability to modulate protein classes that would not be amenable to traditional drug discovery approaches, glue degraders hold the promise of unlocking a large proportion of the undruggable target space and delivering innovative therapies for diseases with high medical need. The lack of scalable discovery strategies has however so far hindered the full exploitation of the clinical potential of molecular glue degraders.

By streamlining and fully integrating cutting-edge genomic, proteomic, and biochemical technologies, Proxygen has successfully developed a highly versatile glue degrader discovery engine. The ligase-agnostic screening approach enables the specific and unbiased identification of molecular glue degraders against difficult-to-drug or completely undruggable targets at large scale. The vast amounts of know-how and data generated in the discovery and chemical optimization of degrader molecules continuously improve the understanding of this novel modality and contribute to Proxygen’s pioneering role in the molecular glue degrader space.

On June 2, 2022 OnKure, Inc., a clinical-stage biopharmaceutical company discovering and developing the next generation of oncology precision medicines, reported that the first patient has been dosed in the Phase 1b/2 Nautilus trial of OKI-179, the Company’s oral Class I histone deacetylase (HDAC) inhibitor, in combination with binimetinib (MEKTOVI), Pfizer’s MEK inhibitor, in patients with advanced NRAS-mutated melanoma (Press release, OnKure, JUN 2, 2022, View Source;utm_medium=rss&utm_campaign=onkure-therapeutics-announces-first-patient-dosed-in-the-phase-1b-2-nautilus-trial-of-oki-179-in-combination-with-binimetinib-in-patients-with-advanced-nras-mutated-melanoma [SID1234615437]).

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"We are pleased to advance the clinical development of our lead candidate, OKI-179, and for the first time, investigate its potential in combination with a MEK inhibitor," said Jennifer Diamond, M.D., Chief Medical Officer of OnKure. "The combination of HDAC inhibition with MEK inhibition is synthetically lethal in RAS-pathway mutated cancers, resulting in increased tumor regressions by inducing DNA damage that is not seen with either agent alone. Given the favorable safety and tolerability profile of OKI-179, we believe its synergistic combination with binimetinib has the potential to be an effective treatment option for patients diagnosed with this highly aggressive melanoma."

The Phase 1b/2 Nautilus study is an open-label, dose-escalation and expansion trial designed to determine the safety and efficacy of OKI-179 combined with binimetinib in patients with NRAS-mutated melanoma. OKI-179 will be administered on a 4 days on/3 days off schedule, with binimetinib administered BID continuously. The Phase 1b portion of this study will determine the maximum tolerated dose, the dose-limiting toxicities, and the recommended Phase 2 dose (RP2D) of OKI-179 and binimetinib in patients with RAS-pathway mutated solid tumors. The Phase 2 portion of the trial is designed as a Simon’s optimal 2-stage study that will investigate the efficacy of the combination of OKI-179 and binimetinib at the RP2D in patients with previously treated NRAS-mutated melanoma. For more information about the study, please visit www.clinicaltrials.gov (NCT05340621).

About NRAS-Mutated Melanoma
NRAS is the second most common oncogenic driver in melanoma, accounting for 20% of all melanomas. Tumors bearing NRAS mutations are more aggressive and are associated with poorer patient outcomes. Despite the prevalence of NRAS mutations and the severity of the resulting disease, treatment options for NRAS-mutated melanoma remain limited, with little efficacy.

About OKI-179
OKI-179 is a novel, oral Class I histone deacetylase (HDAC) inhibitor for the potential treatment of a wide range of solid and hematological malignancies. HDAC inhibitors have shown great promise in preclinical models, however they have had little success treating solid tumors, often due to poor tolerability, inappropriate dosing regimens, poorly conceived combinations, and a lack of stratifying biomarkers. OKI-179 is designed to have improved potency, selectivity, tolerability, as well as easy combinability to overcome the historic limitations of other HDAC inhibitors.