On December 1, 2024 Ensem Therapeutics, Inc. (ENSEM), a pioneering drug discovery and development company that leverages its unique Kinetic Ensemble platform to advance innovative small molecule precision medicines for oncology, reported the first presentation of preclinical data on ETX-636, a potential best-in-class novel allosteric pan-mutant-selective PI3Kα inhibitor and degrader (Press release, ENSEM Therapeutics, DEC 10, 2024, View Source [SID1234649019]). ETX-636 has a differentiated preclinical profile and the potential to deliver clinical benefit to patients with tumors harboring all forms of mutant PI3Kα. The ETX-636 preclinical data is being presented in a poster session during the 47th Annual San Antonio Breast Cancer Symposium ("SABCS") in San Antonio, Texas, on Dec. 12.

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PI3Kα is among the most frequently mutated oncogenes, with activating mutations seen in approximately 16 percent of all tumors and up to 40 percent of hormone receptor positive/HER2-negative advanced breast cancer. However, wildtype PI3Kα is also central to glucose homeostasis and ATP-binding-site orthosteric inhibitors target both mutant and wildtype PI3Kα, resulting in hyperglycemia which limits the clinical utility of these therapeutics.

ETX-636 is a novel orally bioavailable allosteric pan-mutant-selective PI3Kα inhibitor and degrader. This dual mechanism of action results in deep and durable pathway inhibition and induces concordant tumor regression in kinase and helical domain PI3Kα-mutant breast cancer xenografts without inducing wildtype PI3Kα inhibition-mediated hyperglycemia or other toxicities. Additionally, in an ER-positive, HER2-negative, PI3Kα-mutant breast cancer xenograft, ETX-636 is efficacious as a single agent and shows synergistic activity with the standard-of-care agent fulvestrant. ENSEM believes this molecule will significantly improve outcomes for patients with PI3Kα mutations, whether in cancer or rare diseases.

"The promising preclinical results with ETX-636 underscore the potential of our Kinetic Ensemble platform to discover small molecules against high value and difficult to drug targets," said Shengfang Jin, CEO and Co-Founder of ENSEM. "Targeting mutant PI3Kα within tumors while sparing wildtype PI3Kα in normal tissues represents a significant clinical challenge. ETX-636 is a potent mutant-specific allosteric PI3Kα inhibitor and degrader which differentiates it from other compounds in its class." She noted that ETX-636 is completing IND-enabling studies with a first-in-human clinical trial anticipated in the first half of 2025. ENSEM will evaluate ETX-636 as a monotherapy and in combinations with standard-of-care agents in cancer patients harboring PI3Kα mutations.

Poster Details

Title: ETX-636, a Potential Best-In-Class, Oral Small Molecule Allosteric Pan-Mutant-Selective PI3Kα Inhibitor and Degrader
Poster ID: P4-12-18
Sessions: Poster Session 4
Date/Time: Thursday, December 12, 2024, from 5:30 to 7 p.m. CT
Location: Halls 2-3

On December 10, 2024 Scorpion Therapeutics, Inc. ("Scorpion"), a clinical-stage, precision oncology company developing transformational targeted therapies for patients with cancer, reported updated analyses from its Phase 1/2 study of STX-478 in advanced solid tumor patients in a poster spotlight presentation at the San Antonio Breast Cancer Symposium ("SABCS") 2024 and provided program updates, including a new collaboration with Pfizer to evaluate the triplet combination of STX-478 + atirmociclib + fulvestrant in frontline patients with PI3Kα-mutated HR+/HER2- metastatic breast cancer (Press release, Scorpion Therapeutics, DEC 10, 2024, View Source [SID1234649018]).

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"Scorpion is dedicated to expanding the reach of precision medicine to as many patients as quickly as possible. Our updated analyses presented at SABCS show STX-478’s low dose modification rates and increased response rate at higher doses, reflecting its high level of pathway inhibition. These studies, along with our new collaboration with Pfizer to advance the triplet study of STX-478 + fulvestrant with their novel, selective investigative CDK4 inhibitor in frontline patients, bring us one step closer to this ambitious goal," said Adam Friedman, M.D., Ph.D., Chief Executive Officer of Scorpion. "We are committed to being at the forefront of the emerging treatment landscape as we actively enroll our fulvestrant +/- CDK4/6 inhibitors cohorts of STX-478 and explore new triplet combinations with promising next-generation therapies such as atirmociclib."

Expansion Study Collaboration Updates

Scorpion Therapeutics and Pfizer Inc. (NYSE: PFE) entered into a new clinical trial collaboration and supply agreement to evaluate atirmociclib, Pfizer’s investigative selective-CDK4 inhibitor, in combination with STX-478 and fulvestrant in patients with PI3Kα-mutated, HR+/HER2- metastatic breast cancer in the frontline metastatic setting. Under the terms of the agreement, Scorpion and Pfizer will equally share the development costs of the study. In addition, Pfizer will supply atirmociclib for use in the study and Scorpion will manage the conduct of the study. The STX-478 + atirmociclib + fulvestrant triplet combination is planned to begin in 2H25.

Data from the Phase 1/2 Study of STX-478 in Advanced Solid Tumors at SABCS 2024

Scorpion has shown in Phase 1 monotherapy data that STX-478, an oral, once-daily, mutant-selective, allosteric PI3Kα inhibitor, demonstrated robust PI3Kα pathway inhibition as a monotherapy, with anti-tumor activity observed in multiple cancer types, including a 23% overall response rate (ORR) in HR+/HER2- breast cancer (BC) and a 44% ORR in gynecological tumors, amongst others. STX-478 was well-tolerated, including in pre-diabetic, diabetic and heavily pre-treated patients and showed minimal significant wild-type-mediated toxicities. These results suggest that STX-478 could overcome the limitations of currently available pathway inhibitors and, consequently, meaningfully improve clinical outcomes for patients with PI3Kα kinase or helical domain-mutated solid tumors.

In the poster presented at SABCS 2024, updated analyses for STX-478 demonstrated a favorable safety profile with minimal dose modifications observed, including no patient discontinuations due to an adverse event. Updated efficacy analyses demonstrated a positive dose-response relationship as monotherapy in patients with HR+/HER2- breast cancer, which correlates with a high level of PI3Kα pathway target coverage. Combination cohorts with a STX-478 + fulvestrant doublet and STX-478 + fulvestrant + CDK4/6 inhibitor triplet are actively enrolling in patients with HR+/HER2- breast cancer.

The presentation is available here on Scorpion’s website.

"STX-478 is characterized by a markedly higher therapeutic index, improving clinical outcomes and quality of life for patients during treatment compared to approved non-mutant-selective inhibitors," said Dejan Juric, M.D., Director of the Termeer Center for Targeted Therapies at the Massachusetts General Hospital and STX-478 trial investigator. "Based on the very promising monotherapy results, I look forward to studying STX-478’s activity in doublet and triplet combination trials, particularly those that capture the known synergy between inhibition of PI3Kα and estrogen receptor antagonism in HR+/HER2-breast cancer, as well as CDK inhibition. Development of higher order combinations of increasingly selective targeted therapeutic agents represents the next frontier in precision oncology, and I believe STX-478 is well-positioned to drive major progress in this area."

About STX-478

STX-478 is an allosteric, wild-type-sparing, CNS-penetrant, oral small molecule inhibitor of mutant PI3Kα, a well-known, clinically-validated oncogene associated with a variety of solid tumors and one of the most highly mutated targets in all of cancer, which occurs in more than 166,000 patients per year with breast, gynecological and other solid tumors in the United States alone. Based on preclinical data and initial data from the ongoing Phase 1/2 trial, STX-478 has the potential to address significant unmet needs in patients with PI3Kα-mutant cancers left by existing therapies through less toxicity and sustained and deeper responses. STX-478 is in an ongoing Phase 1/2 trial exploring its activity across a range of solid tumors with both kinase and helical domain mutations. The trial includes patients both previously exposed to and naïve to alpelisib and other PI3K pathway inhibitors and includes expansion cohorts in which STX-478 is being evaluated in combination with fulvestrant in second line HR+/HER2- breast cancer and in combination with fulvestrant plus CDK4/6 inhibitors in frontline HR+/HER2- breast cancer. To learn more about the first-in-human trial of STX-478, please visit this page.

On December 10, 2024 Ensem Therapeutics, Inc. (ENSEM), a pioneering drug discovery and development company that leverages its unique Kinetic Ensemble platform to advance innovative small molecule precision medicines for oncology, reported for the first time preclinical data on ETX-197/BG-68501, a potential best-in-class oral, selective CDK2 inhibitor at the 47th Annual San Antonio Breast Cancer Symposium ("SABCS") in San Antonio, Texas (Press release, ENSEM Therapeutics, DEC 10, 2024, View Source [SID1234649017]). ETX-197/BG-68501 has a differentiated preclinical profile and the potential to deliver clinical benefit to patients with tumors associated with CDK2 dependency.

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CDK2 is a well-established vulnerability of multiple cancers, including tumors with increased expression of Cyclin E (CCNE) or the mutation/loss of the Retinoblastoma 1 gene (RB1). There are currently no approved CDK2 specific drugs. ETX-197/BG-68501 was designed through ENSEM’s Kinetic Ensemble platform to induce previously unexplored interactions within the CDK2 ATP binding pocket, leading to increased potency and selectivity compared to other CDK2 inhibitors.

ETX-197/BG-68501 shows tight binding (slow off-rate) for CDK2 which results in potent and concordant pharmacodynamic modulation and anti-proliferative activity both in vitro and in vivo. ETX-197/BG-68501 is 100-fold more selective for CDK2 over other kinases in the CDK family and this superior selectivity extends more broadly against 385 other kinases, indicating the potential for promising tolerability in the clinic.

In mouse xenograft studies using a CCNE-amplified ovarian cancer cell line or patient-derived tumors, ETX-197/BG-68501 showed sustained target engagement, dose-dependent tumor growth inhibition with excellent tolerability. ETX-197/BG-68501 demonstrated single agent efficacy in a breast cancer xenograft model that had acquired resistance to a CDK4/CDK6 inhibitor. In addition, ETX-197/BG-68501 showed anti-tumor activity in other in vitro and in vivo tumor models including small cell lung and ovarian cancers, indicating its broad clinical potential beyond breast cancer.

"Inhibiting CDK2 potently and selectively over other CDK family members represents a significant challenge," said Shengfang Jin, CEO and Co-Founder of ENSEM. "The promising preclinical results with ETX-197/BG-68501 underscore the potential of our Kinetic Ensemble platform to discover small molecules against high value and difficult to drug targets." She noted that BeiGene is currently conducting a first-in-human Phase 1a/1b clinical study (NCT06257264) to assess the safety tolerability, pharmacokinetics, pharmacodynamics and preliminary anti-tumor activity of ETX-197/BG-68501, and is presenting a "Trial-in-Progress" poster for this ETX-197/BG-68501 clinical study at the Symposium.

Poster Details

Title: ETX-197/BG-68501, a potential best-in-class potent, selective oral small molecule CDK2 inhibitor, has anti-tumor activity in cancer models with Cyclin E amplification or deficiency in the Retinoblastoma 1 gene
Poster ID: P4-12-29
Sessions: Poster Session
Date/Time: Thursday, December 12, 2024, from 5:30 to 7 p.m. CT
Location: Halls 2-3

On December 10, 2024 BostonGene, a leading provider of AI-driven molecular and immune profiling solutions, reported that three abstracts have been accepted for poster presentations at the 2024 San Antonio Breast Cancer Symposium (SABCS), to take place December 10 – 13, 2024, at the Henry B. Gonzalez Convention Center in San Antonio, Texas (Press release, BostonGene, DEC 10, 2024, View Source [SID1234649016]). BostonGene will also exhibit at booth 1317.

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"We’re excited to present our research at the 2024 SABCS, underscoring BostonGene’s commitment to leveraging molecular profiling as a transformative tool in breast cancer treatment," said Nathan Fowler, MD, Chief Medical Officer at BostonGene. "Our findings in transcriptomic classification aim to pave the way for more effective treatment pathways, establishing new benchmarks for precision oncology."

Details about the abstracts selected for presentation are below:

Abstract number: 1760
Title: Evaluating the Correlation Between FISH and NGS in Assessing ERBB2 Alterations in Breast Cancer
Date & time: Wednesday, December 11 | 12:00 PM – 2:00 PM
Presenter: Nikita Kotlov, BostonGene

This comparative analysis demonstrated the utility of NGS in evaluating ERBB2 (HER2) status in breast cancer compared to the gold standard, fluorescence in situ hybridization (FISH). NGS detected potentially clinically relevant ERBB2 mutations in non-amplified samples. With enhanced resolution, NGS also revealed heterogeneity among ERBB2 (HER2) amplifications in breast cancer. Identifying these nuanced genomic and transcriptomic alterations yields valuable insights for designing personalized treatment strategies for breast cancer patients.

Abstract number: 2476
Title: Comprehensive Analysis of ADC Target Expression in Invasive Lobular Carcinoma
Date & time: Wednesday, December 11 | 12:00 PM – 2:00 PM
Presenter: Jason Mouabbi, MD, The University of Texas MD Anderson Cancer Center

RNA-seq was applied to examine 82 cell surface proteins as potential antibody-drug conjugate (ADC) targets in invasive lobular carcinoma (ILC). Distinct expression landscapes of the prospective ADC targets were present across different ILC subtypes. These findings underscore the need to account for varied ADC target expression landscapes across ILC subtypes for optimal efficacy and safety of ADC-based treatments.

Research done in collaboration with MD Anderson Cancer Center

Abstract number: 1521
Title: Levels of Circulating Tumor DNA as a Predictive Marker for Early Switch in Treatment for Patients with Metastatic Breast Cancer: A Phase 2 Randomized, Open-Label Study
Date & time: Thursday, December 12 | 5:30 PM – 7:00 PM
Presenter: Frances Valdes, MD, University of Miami

This phase 2 randomized, open-label study compares patients with metastatic breast cancer receiving a CDK4/6 inhibitor combined with either an aromatase inhibitor or fulvestrant as first-line therapy. BostonGene’s liquid biopsy test was incorporated to validate the clinical utility of serial circulating tumor (ctDNA) for patient monitoring. Capable of detecting molecular progression before clinical manifestation, levels of ctDNA were predictive for early switch in treatment in metastatic breast cancer patients. While analysis and patient monitoring are ongoing, this study has yielded clinically relevant genomic findings that may shed light on strategies to extend the duration of disease control and prolong patient survival.

Research done in collaboration with the University of Miami

On December 10, 2024 Incyte (Nasdaq:INCY) reported additional results from the pivotal Phase 3 inMIND trial evaluating treatment with tafasitamab (Monjuvi), a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody, in combination with lenalidomide and rituximab compared with placebo plus lenalidomide and rituximab in patients with relapsed or refractory follicular lymphoma (FL) (Press release, Incyte, DEC 10, 2024, View Source [SID1234649015]). These data are featured today in the Late-breaking Session (LBA-1) at the 2024 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in San Diego.

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The late-breaking results, which build on previously announced topline data, show that the study met its primary endpoint by demonstrating a statistically significant and clinically meaningful improvement in progression-free survival (PFS) by investigator assessment in 548 patients with FL. Patients treated with tafasitamab achieved a median PFS by investigator assessment of 22.4 months compared to 13.9 months in the control arm (Hazard Ratio [HR]: 0.43; 95% Confidence Interval [CI] (0.32—0.58); P<0.0001), representing a 57% reduction in risk of progression, relapse, or death. The PFS assessed by an Independent Review Committee (IRC) was consistent with investigator-based results, with a HR of 0.41 (95% CI 0.29, 0.56, P<0.0001). Median PFS by IRC was not reached in the tafasitamab group versus 16.0 months in the control arm, [95% CI (19.3-NE) and (13.9, 21.1), respectively; P<0.0001]. The PFS benefit was consistent across all patient subgroups regardless of the number of previous lines of therapy.

"In the Phase 3 inMIND trial, tafasitamab demonstrated impressive efficacy and safety for treating certain patients with follicular lymphoma, the most common type of B-cell non-Hodgkin lymphoma," said Steven Stein, M.D., Chief Medical Officer, Incyte. "These data, the first to evaluate the novel approach of combining CD19 and CD20 immunotherapies, show the potential of tafasitamab in combination with lenalidomide and rituximab to become a new standard of care for these patients. We look forward to working with regulatory authorities to potentially bring this treatment forward to patients with FL."

The trial also showed improvement across secondary endpoints, including:

Complete response (CR), overall response rate (ORR) and duration of response (DOR) each showed improvement in the tafasitamab group versus the control arm (CR of 49.4% vs. 39.8% [95% CI (43.1, 55.8) and (33.7, 46.1), respectively; OR=1.5, P=0.0286); (ORR of 83.5% vs. 72.4% [95% CI (78.6, 87.7) and (66.7, 77.6), respectively]); (DOR of 21.2 months vs. 13.6 months [95% CI (19.5—NE) and (12.4—18.6), respectively]).
Median overall survival (OS) was not reached in either group, but a positive trend was observed with the tafasitamab group versus the control arm (HR=0.59 [95% CI (0.31, 1.13)]).
Additionally, median time to next treatment (TTNT) was not reached in the tafasitamab group and was 28.8 months in the control arm (HR [95% CI], 0.45 [0.31, 0.64], nominal P<0.0001).

Tafasitamab was generally well-tolerated, and safety was consistent with other CD19 and immunotherapy combination regimens. The most common treatment-emergent adverse events (TEAEs) in the tafasitamab and immunotherapy combination group were neutropenia (48.5%), diarrhea (37.6%), COVID-19 (31.4%) and constipation (29.2%).

"Patients with follicular lymphoma have a high risk of relapse, yet there are limited treatment options in the relapsed and refractory setting," said Dr. Laurie Sehn, British Columbia Cancer Centre for Lymphoid Cancer. "The goal of therapy is primarily to prolong remission, while maintaining quality of life. The inMIND trial demonstrated a meaningful improvement in disease control with the addition of the anti-CD19 monoclonal antibody tafasitamab to lenalidomide and rituximab, providing patients with a new, well tolerated, immunotherapy combination."

About inMIND
A global, double-blind, randomized, controlled Phase 3 study, inMIND (NCT04680052) evaluated the clinical benefit of tafasitamab and lenalidomide as an add-on to rituximab compared with lenalidomide alone as an add-on to rituximab in patients with relapsed or refractory follicular lymphoma (FL) Grade 1 to 3a or relapsed or refractory nodal, splenic or extranodal marginal zone lymphoma (MZL). The study enrolled a total of 654 adults (age ≥18 years).

The primary endpoint of the study is progression-free survival (PFS) by investigator assessment in the FL population, and the key secondary endpoints are PFS in the overall population as well as positron emission tomography complete response (PET-CR) and overall survival (OS) in the FL population.

For more information about the study, please visit View Source

About Tafasitamab (Monjuvi)
Tafasitamab (Monjuvi) is a humanized Fc-modified cytolytic CD19 targeting monoclonal antibody. In 2010, MorphoSys licensed exclusive worldwide rights to develop and commercialize tafasitamab from Xencor, Inc. Tafasitamab incorporates an XmAb engineered Fc domain, which mediates B-cell lysis through apoptosis and immune effector mechanism including Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC) and Antibody-Dependent Cellular Phagocytosis (ADCP). MorphoSys and Incyte entered into: (a) in January 2020, a collaboration and licensing agreement to develop and commercialize tafasitamab globally; and (b) in February 2024, an agreement whereby Incyte obtained exclusive rights to develop and commercialize tafasitamab globally.

In the United States, Monjuvi (tafasitamab-cxix) received accelerated approval by the U.S. Food and Drug Administration in combination with lenalidomide for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified, including DLBCL arising from low grade lymphoma, and who are not eligible for autologous stem cell transplant (ASCT). In Europe, Minjuvi (tafasitamab) received conditional Marketing Authorization from the European Medicines Agency in combination with lenalidomide, followed by Minjuvi monotherapy, for the treatment of adult patients with relapsed or refractory DLBCL who are not eligible for ASCT.

XmAb is a registered trademark of Xencor, Inc.

Monjuvi, Minjuvi, the Minjuvi and Monjuvi logos and the "triangle" design are registered trademarks of Incyte.

IMPORTANT SAFETY INFORMATION

What are the possible side effects of MONJUVI?
MONJUVI may cause serious side effects, including:

Infusion reactions. Your healthcare provider will monitor you for infusion reactions during your infusion of MONJUVI. Tell your healthcare provider right away if you get fever, chills, flushing, headache, or shortness of breath during an infusion of MONJUVI.
Low blood cell counts (platelets, red blood cells, and white blood cells). Low blood cell counts are common with MONJUVI, but can also be serious or severe. Your healthcare provider will monitor your blood counts during treatment with MONJUVI. Tell your healthcare provider right away if you get a fever of 100.4°F (38°C) or above, or any bruising or bleeding.
Infections. Serious infections, including infections that can cause death, have happened in people during treatment with MONJUVI and after the last dose. Tell your healthcare provider right away if you get a fever of 100.4°F (38°C) or above, or develop any signs and symptoms of an infection.
The most common side effects of MONJUVI include:

Feeling tired or weak
Diarrhea
Cough
Fever
Swelling of lower legs or hands
Respiratory tract infection
Decreased appetite
These are not all the possible side effects of MONJUVI. Your healthcare provider will give you medicines before each infusion to decrease your chance of infusion reactions. If you do not have any reactions, your healthcare provider may decide that you do not need these medicines with later infusions. Your healthcare provider may need to delay or completely stop treatment with MONJUVI if you have severe side effects.

Before you receive MONJUVI, tell your healthcare provider about all of your medical conditions, including if you:

Have an active infection or have had one recently.
Are pregnant or plan to become pregnant. MONJUVI may harm your unborn baby. You should not become pregnant during treatment with MONJUVI. Do not receive treatment with MONJUVI in combination with lenalidomide if you are pregnant because lenalidomide can cause birth defects and death of your unborn baby.
You should use an effective method of birth control (contraception) during treatment and for at least 3 months after your final dose of MONJUVI.
Tell your healthcare provider right away if you become pregnant or think that you may be pregnant during treatment with MONJUVI.
Are breastfeeding or plan to breastfeed. It is not known if MONJUVI passes into your breastmilk. Do not breastfeed during treatment for at least 3 months after your last dose of MONJUVI.
You should also read the lenalidomide Medication Guide for important information about pregnancy, contraception, and blood and sperm donation.

Tell your healthcare provider about all the medications you take, including prescription and over-the-counter medicines, vitamins, and herbal supplements.

Call your doctor for medical advice about side effects. You may report side effects to the FDA at (800) FDA-1088 or www.fda.gov/medwatch. You may also report side effects to Incyte Medical Information at 1-855-463-3463.

Please see the full Prescribing Information for Monjuvi, including Patient Information, for additional Important Safety Information.