Blueprint Medicines Announces BLU-945 Proof-of-Concept Data Supporting Initiation of Comprehensive Combination Development Strategy in EGFR-mutant Non-Small Cell Lung Cancer

On April 8, 2022 Blueprint Medicines Corporation (NASDAQ: BPMC) reported proof-of-concept data from the Phase 1/2 SYMPHONY clinical trial of BLU-945, an investigational precision therapy for advanced EGFR-mutant non-small cell lung cancer (NSCLC) (Press release, Blueprint Medicines, APR 8, 2022, View Source [SID1234611727]). The trial results showed early evidence of safety and clinical activity consistent with preclinical data, supporting plans to expand development of BLU-945 in combination with multiple agents including osimertinib, with the goal of preventing or treating tumor resistance to prolong patient benefit. The data were reported today at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022 in New Orleans.

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Early data from the ongoing Phase 1 dose escalation part of the SYMPHONY trial showed dose-dependent decreases in circulating tumor DNA (EGFR variant allele fractions) and radiographic tumor reductions, including a partial response (PR) in a patient treated with 400 mg once daily (QD), the highest dose tested as of the data cutoff date. Pharmacokinetic results showed BLU-945 exposures at higher doses were associated with broad EGFR mutation coverage, including the activating L858R mutation with or without the osimertinib-resistant C797S mutation. BLU-945 was generally well-tolerated, with no significant adverse events (AEs) associated with wild-type EGFR inhibition. The maximum tolerated dose and recommended Phase 2 dose have not yet been identified, and dose escalation is continuing.

"Today, targeted therapies are the mainstay treatment for EGFR-mutant lung cancer, but tumor resistance emerges in the majority of patients, driving mutational heterogeneity and disease progression. Innovative treatment strategies, including targeted therapy combinations, are urgently needed to prevent or treat this mutational heterogeneity and prolong patient benefit," said Elaine Shum, M.D., assistant professor in the Department of Medicine and a medical oncologist at NYU Langone Health’s Perlmutter Cancer Center, and an investigator on the SYMPHONY trial. "The initial BLU-945 data reported today, which highlight its potential to address resistance to current standard of care therapies including osimertinib and enable well-tolerated, broad-acting combinations, are an important step forward toward improving outcomes for patients with EGFR-mutant lung cancer."

"We believe BLU-945 is distinguished from other EGFR-directed therapies, based on its ability to inhibit the most difficult-to-target EGFR mutations while maintaining a wide therapeutic index over wild-type EGFR, a known driver of toxicity. As a result, BLU-945 has significant potential as a combination partner with other targeted therapies and broad-acting agents," said Fouad Namouni, M.D., President, Research & Development at Blueprint Medicines. "We are excited to see the preclinical profile of BLU-945 translated in the clinic, with early dose escalation data showing evidence of clinical activity, broad EGFR mutation coverage and tolerability. Based on these promising data, we plan to rapidly expand development of BLU-945 in combination with osimertinib and other agents to address important medical needs across all lines of therapy."

Blueprint Medicines is initiating a SYMPHONY trial cohort assessing BLU-945 in combination with osimertinib in patients with second-line or later EGFR-mutant NSCLC, following disease progression on osimertinib. After the selection of a recommended Phase 2 combination dose regimen, the company plans to initiate an expansion cohort with registration potential in biomarker-selected second-line patients, as well as an expansion cohort in front-line patients, by the end of 2022. Additional combinations with BLU-701, chemotherapy and antibody-drug conjugate therapy are planned across multiple mutation profiles and lines of therapy.

In addition, Blueprint Medicines announced today a clinical trial supply agreement with AstraZeneca (LSE/STO/Nasdaq: AZN). Under the terms of the agreement, Blueprint Medicines will evaluate BLU-945 and BLU-701 in combination with osimertinib in the ongoing SYMPHONY and HARMONY trials, respectively.

BLU-945: Data from the Phase 1/2 SYMPHONY Trial

As of a data cutoff date of March 9, 2022, 33 patients with EGFR-mutant NSCLC have been treated with BLU-945 across five dose escalation cohorts (range: 25-400 mg QD). The majority of patients (79 percent) previously received at least three lines of systemic therapy, including osimertinib (97 percent). Patient eligibility criteria require the presence of an EGFR mutation based on local assessment of tumor biopsy or circulating tumor DNA (ctDNA).

BLU-945 was generally well-tolerated at all doses tested. The most common AEs (regardless of relationship to BLU-945; ≥10 percent) were nausea, headache, fatigue, cough, dyspnea, vomiting, hyponatremia, dry mouth and anemia. Reported AEs associated with wild-type EGFR inhibition were infrequent and low grade, including rash (one patient; Grade 1) and diarrhea (three patients; all Grade 1). One dose-limiting toxicity (Grade 3 transaminitis) occurred in the 400 mg QD cohort, which improved with dose interruption. There were no treatment discontinuations due to AEs.

Pharmacokinetic data showed dose-proportional plasma concentrations, with exposures at increasing doses consistent with broad EGFR mutation coverage, based on preclinical activity thresholds. Mean plasma exposures at doses of 100 mg QD or higher exceeded the IC90 for mutants harboring the T790M and C797S resistance mutations, regardless of activating mutation. In addition, mean plasma exposure at 400 mg QD exceeded the IC90 for mutants harboring the activating L858R mutation with or without the C797S mutation.

The SYMPHONY trial is one of the first oncology studies to analyze plasma ctDNA via real-time next-generation sequencing to assess tumor biology and early drug activity. Results for patients with detectable T790M and C797S allele fractions at baseline and available post-baseline assessments showed dose-dependent reductions in both variant allele fractions. In patients treated with 400 mg QD, all detectable T790M and C797S allele fractions declined, including three that fell below the limit of detection (clearance).

Patients with measurable target lesions at baseline and at least one post-baseline scan were evaluable per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. In a heavily pre-treated population, higher BLU-945 doses led to increased antitumor activity. Tumor shrinkage was observed in patients treated with 200-400 mg QD, including an unconfirmed PR1 in a patient treated with 400 mg QD. This patient had NSCLC harboring exon 19 deletion, T790M and C797S mutations, and previously received platinum-based chemotherapy, erlotinib and osimertinib with a best response of stable disease.

Copies of Blueprint Medicines data presentations from the AACR (Free AACR Whitepaper) annual meeting, including the SYMPHONY trial presentation, are available in the "Science–Publications and Presentations" section of the company’s website at www.blueprintmedicines.com.

Investor Conference Call Information

Blueprint Medicines will host a live webcast today, April 8, 2022 beginning at 2:00 p.m. ET, to discuss the data reported at AACR (Free AACR Whitepaper). To access the live call, please dial 844-200-6205 (domestic) or 929-526-1599 (international), and refer to conference ID 084402. A webcast of the conference call will be available 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.

About Blueprint Medicines’ Clinical Development Programs in EGFR-Mutant NSCLC

Blueprint Medicines is developing three investigational agents, BLU-701, BLU-945 and BLU-451, with the goal of addressing nearly all activating mutations (>90 percent) in EGFR-mutant NSCLC. The introduction of EGFR-targeted therapies, including osimertinib, has transformed the care of patients with EGFR-mutant NSCLC; however, there is a significant need for new treatment options designed to prevent or treat a broad range of resistance mechanisms before they emerge, with the goal of prolonging patient benefit. There are no approved targeted therapies for patients with disease progression following osimertinib, and limited treatment options for patients with EGFR exon 20 insertion-positive NSCLC.

BLU-701 and BLU-945 were designed to provide broad coverage of common activating and on-target resistance mutations, spare wild-type EGFR and other kinases to help limit off-target toxicities, and prevent or treat central nervous system (CNS) metastases. These preclinical profiles may enable BLU-701 and BLU-945 to become the backbones of a range of combination strategies across lines of therapy. The Phase 1/2 SYMPHONY trial (NCT04862780) of BLU-945 and the Phase 1/2 HARMONY trial (NCT05153408) of BLU-701 are currently ongoing for patients with EGFR-mutant NSCLC.

BLU-451 is a selective and potent inhibitor of EGFR exon 20 insertion-positive NSCLC. Based on preclinical data, BLU-451 potently inhibited all common EGFR exon 20 insertion variants with marked selectivity over wild-type EGFR and off-target kinases, and has shown CNS penetration. Blueprint Medicines has initiated a Phase 1/2 trial of BLU-451 (NCT05241873) in EGFR exon 20 insertion-positive NSCLC.

Oncolytics Biotech® Presents New Data Demonstrating Durable Clinical Benefit in Relapsed/Refractory Multiple Myeloma Patients at the AACR Annual Meeting

On April 8, 2022 Oncolytics Biotech Inc. (NASDAQ: ONCY) (TSX: ONC) reported the publication of an electronic poster at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting featuring new clinical biomarker data from a completed investigator-sponsored phase 1b trial of pelareorep and the proteasome inhibitor bortezomib in relapsed/refractory multiple myeloma patients (Press release, Oncolytics Biotech, APR 8, 2022, View Source [SID1234611726]).

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"The results from this trial provide a powerful example of how pelareorep’s immunologic effects trigger a durable clinical benefit in an extremely challenging patient population," said Thomas Heineman, M.D., Ph.D., Chief Medical Officer of Oncolytics Biotech Inc. "All patients enrolled into the study had failed prior therapies, yet despite this, treatment with pelareorep-based therapy prevented disease progression for over three years in a subset of the patients. In addition, this study shows that pelareorep’s ability to recruit high concentrations of anti-cancer immune cells into the tumor microenvironment (TME) can yield strong clinical outcomes. This impressive finding has implications for cancers beyond multiple myeloma as it builds on existing data that support pelareorep’s potential to enhance the effectiveness of a wide array of therapies through its ability to stimulate a pro-inflammatory TME."

Previously reported data highlighted in the poster’s corresponding abstract demonstrated the efficacy of the studied combination and showed a subset of trial participants achieving prolonged progression-free survival (PFS) of greater than three years (link to PR). These data also demonstrate a clinical response correlating with changes in T cell clonality and post-treatment increases in innate and adaptive immune cells within the TME. New biomarker analyses featured in the poster show these anti-cancer immune cells clustering more closely around cancer cells containing pelareorep compared to those that did not. Collectively, these results indicate that the sustained clinical benefits observed were driven by pelareorep’s recruitment of anti-cancer immune cells into the TME.

Dr. Matt Coffey, President and Chief Executive Officer of Oncolytics Biotech Inc., commented, "This trial generated important proof-of-concept data that reaffirm pelareorep’s favorable safety profile, increase our understanding of its mechanism of action, and further support the use of T cell clonality as a biomarker. These important learnings strengthen the systemic effect observed in other datasets supporting each of our clinical programs and can be applied to accelerate their advancement. Moving forward, we plan to use our findings in multiple myeloma to drive conversations with potential partners and collaborators interested in leveraging pelareorep’s immunotherapeutic effects to address unmet needs in this and other indications. Internally, we remain primarily focused on our lead breast cancer program and look forward to its expected randomized phase 2 data readout in the fourth quarter of the year."

The electronic AACR (Free AACR Whitepaper) poster, entitled, Single Cell Analysis Shows That Reovirus Immune Priming Changes the Tumor Immune Micro Environment in Multiple Myeloma, is available to registered attendees of the AACR (Free AACR Whitepaper) annual meeting on the meeting website (Abstract #6354). A copy of the poster will also be posted to the Posters & Publications page of Oncolytics’ website (LINK) following the conclusion of the meeting.

Merus Presents Preclinical Data on MCLA-129 at the American Association for Cancer Research Annual Meeting 2022

On April 8, 2022 Merus N.V. (Nasdaq: MRUS) ("Merus", "the Company", "we", or "our"), a clinical-stage oncology company developing innovative, full-length multispecific antibodies (Biclonics and Triclonics), reported that pre-clinical data highlighting the mechanism of action of MCLA-129 (Press release, Merus, APR 8, 2022, View Source [SID1234611725]). The poster, that is currently available virtually, will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022 in New Orleans, Louisiana on Sunday, April 10, 2022.

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"Our preclinical study of MCLA-129 in non-small cell lung cancer cell lines is encouraging and continues to support the phase 1/2 trial, currently in dose escalation," said Dr. Cecile Geuijen, Senior Vice President and Chief Science Officer at Merus. "We look forward to providing a clinical update from that study in the second half of 2022."

MCLA-129
Observations in the preclinical presentation include:

MCLA-129 inhibits ligand-induced EGFR and c-MET receptor dimerization and phosphorylation
MCLA-129 promotes ADCC and ADCP of NSCLC cells
MCLA-129 significantly inhibits growth of a patient-derived EGFR exon20ins tumor in a preclinical xenograft model
These data provide support for the ongoing phase 1/2 study of MCLA-129 in patients with solid tumors, including NSCLC with EGFR exon20ins (Study MCLA-129-CL01, NCT04868877)
The full poster is available on our website.

MCLA-129 is currently enrolling patients in a phase 1/2, open-label clinical trial consisting of dose escalation followed by a planned dose expansion. Primary objectives of phase 1 are to determine the maximum tolerated dose and/or the recommended phase 2 dose, and the objectives of phase 2 are to evaluate safety, tolerability and potential clinical activity in patients with advanced solid tumors. MCLA-129 is subject to a collaboration and license agreement with Betta Pharmaceuticals Co. Ltd. (Betta), which permits Betta to develop MCLA-129 exclusively in China, while Merus retains global rights outside of China. Merus plans to provide a clinical update in the second half of 2022.

About MCLA-129
MCLA-129 is an antibody-dependent cellular cytotoxicity-enhanced Biclonics that is designed to inhibit the EGFR and c-MET signaling pathways in solid tumors. Preclinical data have shown that MCLA-129 can effectively treat TKI-resistant non-small cell lung cancer in xenograft models of cancer. MCLA-129 is designed to have two complementary mechanisms of action: blocking growth and survival pathways to stop tumor expansion and recruitment and enhancement of immune effector cells to eliminate the tumor.

Checkmate Pharmaceuticals Presents Clinical Trial Biomarker Data with Vidutolimod at the 2022 American Association for Cancer Research (AACR) Annual Meeting

On April 8, 2022 Checkmate Pharmaceuticals, Inc. (NASDAQ: CMPI) ("Checkmate"), a clinical stage biotechnology company focused on developing its proprietary technology to harness the power of the immune system to combat cancer, reported the presentation of biomarker signature data from two studies evaluating vidutolimod, a first-in-class, immunostimulatory, noninfectious virus-like particle (VLP) containing a CpG-A Toll-like receptor 9 (TLR9) agonist (Press release, Checkmate Pharmaceuticals, APR 8, 2022, View Source [SID1234611724]). The first study evaluated vidutolimod in patients with advanced anti-PD-(L)1 refractory melanoma who received intratumoral vidutolimod monotherapy or in combination with intravenous pembrolizumab, and the second evaluated patients with anti-PD-(L)1 refractory non-small cell lung cancer (NSCLC) who received vidutolimod and atezolizumab. The objective of these analyses was to identify transcriptional signatures specific to the antitumor activity of treatment with vidutolimod monotherapy or in combination with PD-1 blockade in these two subsets.

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Novel transcriptional signatures associated with antitumor activity in vidutolimod (vidu)-treated patients (pts) with anti-PD-1-refractory melanoma and non-small cell lung cancer (NSCLC) (Abstract #: LB107: NCT03084640 and NCT03438318)

During the 2022 AACR (Free AACR Whitepaper) Late-Breaking Research: Clinical Research 2 Poster Session on Tuesday, April 12 from 9:00am – 12:30pm CT, Art Krieg, M.D., Founder and Chief Scientific Officer of Checkmate, presents analyses of RNA Seq data from baseline biopsies of tumors in patients with anti-PD-1-refractory melanoma and NSCLC.

Key highlights from these clinical trial biomarker data include:

Expression of a 35-gene COPII/Golgi core signature was associated with antitumor activity of intratumoral vidutolimod ± intravenous anti–PD-(L)1. This finding is consistent with published reports that COPII vesicle and Golgi trafficking are critical for TLR9 trafficking and function
Association with response to vidutolimod monotherapy suggests that the COPII/Golgi core signature is linked to effective TLR9 agonism. The signature was independent of tumor inflammation and baseline patient characteristics such as LDH, presence of liver metastases, or tumor burden
Machine learning of the RNA Seq dataset revealed that the COPII/Golgi signature in combination with ELF2 expression provided a stronger differentiation between responders and non-responders to vidutolimod, regardless of baseline tumor inflammation
A macrophage signature was associated with nonresponse in T cell–inflamed melanoma, consistent with other evidence that high concentrations of tumor-associated macrophages (or myeloid-derived suppressor cells) may suppress TLR9 activation by vidutolimod
The presence of these signatures and potential association with clinical response is being evaluated in further RNA Seq datasets being generated from ongoing clinical trials of vidutolimod in combination with various checkpoint inhibitors
"These data suggest that the tumor regression we have seen in patients treated with intratumoral vidutolimod with or without checkpoint inhibitors may be predicted from the presence of one or more novel transcriptional signatures in the baseline tumor biopsies," said Dr. Art Krieg, Founder and Chief Scientific Officer of Checkmate. "These signatures are consistent with what we know about TLR9 biology and they provide clues to possible new combinations and patient populations who may be especially amenable to vidutolimod treatment. We look forward to determining the prevalence of these signatures in other cancers and to exploring the potential for a biomarker-based enrichment strategy across cancer."

Adaptimmune Presents MAGE-A4 Expression Data from its Screening Protocol at AACR Confirming Expression Across a Broad Range of Solid Tumors

On April 8, 2022 Adaptimmune Therapeutics plc (Nasdaq: ADAP), a leader in cell therapy to treat cancer, reported data from the multinational, multicenter, screening protocol (NCT02636855) at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) annual meeting in a poster entitled "Identifying MAGE-A4-Positive Tumors for SPEAR T-Cell Therapies in HLA-A*02–Eligible Patients" (Press release, Adaptimmune, APR 8, 2022, View Source [SID1234611723]).

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"This large clinical dataset continues building the science around MAGE-A4 expression, and provides a broad, real-world understanding of patient eligibility for our clinical trials with SPEAR T-cell therapies targeting MAGE-A4," said Elliot Norry, Adaptimmune’s Chief Medical Officer. "This information confirms the potential of our MAGE-A4 franchise and our continued commitment to patients and clinicians."

The screening protocol prospectively evaluated HLA types and MAGE-A4 expression levels to determine eligibility for the Company’s clinical trials with SPEAR T-cells targeting MAGE-A4 across a broad range of solid tumors. To be eligible, patients are required to be HLA-A*02 positive1 and tumor samples need to meet protocol-defined MAGE-A4 expression levels2 . Data were collected for screening in the Phase 1 trial of afami-cel (formerly ADP-A2M4; closed to enrollment) as well as the ongoing Phase 1 SURPASS trial.

Results from this large dataset are consistent with data previously shared by the Company and support MAGE-A4 as an important cancer target within the tumor types currently included in ongoing clinical trials of afami-cel and ADP-A2M4CD8.

Across sites in the US, Canada, and Spain, a total of 6167 patients had their HLA-A type accurately determined and 2729 (44.3%) were eligible based on protocol-defined criteria. Among HLA-eligible patients, 1543 had tumor samples evaluable for MAGE-A4 with 313 (20%) meeting the requirements for MAGE-A4 expression.

The rate of eligible MAGE-A4 expression levels was highest in synovial sarcoma (67%) and ranged from 20% to 35% across the following solid tumor indications: squamous small cell lung (35%); bladder (32%), esophagogastric junction (26%), ovarian (24%), head and neck squamous cell (22%), and esophageal (21%) cancers.