MorphoSys and I-Mab Announce First Patient Dosed in Phase 3 Clinical Trial of MOR202/TJ202 in r/r Multiple Myeloma in Mainland ChinaMorphoSys AG:

On April 27, 2020 MorphoSys AG (FSE: MOR; Prime Standard Segment, MDAX & TecDAX; NASDAQ: MOR) and I-Mab (NASDAQ: IMAB) reported that the first patient has been dosed in a phase 3 clinical study in mainland China to evaluate MorphoSys’ investigational human CD38 antibody MOR202/TJ202 in combination with lenalidomide plus dexamethasone in patients with relapsed or refractory multiple myeloma (r/r MM) (Press release, MorphoSys, APR 27, 2020, View Source [SID1234556631]). Under a licensing agreement with MorphoSys, I-Mab, a clinical stage biopharmaceutical company committed to discovery, development and commercialization of novel or highly differentiated biologics to treat diseases with significant unmet medical needs, has exclusive rights for development and commercialization of MOR202/TJ202 in mainland China, Taiwan, Hong Kong and Macao.

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The clinical trial (NCT03952091) in mainland China is a randomized, open-label, parallel-controlled, multi-center study to evaluate the efficacy and safety of the combination of MOR202/TJ202, lenalidomide and dexamethasone versus the combination of lenalidomide and dexamethasone in patients with r/r MM who received at least one prior line of treatment. This multi-center study has already started at sites in Taiwan in April 2019 and now officially started in mainland China as part of the coordinated effort to accelerate the study.

"MOR202/TJ202 is a front-runner candidate that adequately demonstrates our fast-to-market development strategy, representing a highly differentiated clinical development approach to provide new treatment options for unmet medical needs," said Dr. Joan Shen, CEO of I-Mab. "The phase 3 study is the second registrational trial of MOR202/TJ202 as a potential second line treatment option for patients with multiple myeloma in Greater China."

"We are delighted that our partner I-Mab has dosed the first patient in the ongoing phase 3 study for MOR202/TJ202 in mainland China, which marks an important step in the development of this compound," commented Dr. Malte Peters, Chief Research & Development Officer of MorphoSys. "There is a high need for the treatment of patients with r/r multiple myeloma in the Greater China area and we look forward to the further development of MOR202/TJ202 by our partner I-Mab in this indication."

In addition to the phase 3 trial, I-Mab is conducting a pivotal phase 2 study (NCT03860038) to evaluate the efficacy and safety of MOR202/TJ202 in combination with dexamethasone in subjects with r/r MM who received at least 2 prior lines of treatment.

About MOR202/TJ202
MOR202/TJ202 is an investigational human monoclonal antibody derived from MorphoSys’s HuCAL antibody technology. The antibody is directed against CD38 on the surface of multiple myeloma cells, which has been characterized as one of the most strongly and uniformly expressed antigens on the surface of malignant plasma cells. According to its suggested mode of action, the antibody recruits cells of the body’s immune system to kill the tumor through antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). The antibody does not involve complement dependent cytotoxicity, or CDC, an additional immune mechanism involved in tumor cell killing. Scientific research suggests that an anti-CD38 antibody may have therapeutic potential also in other cancers as well as autoimmune diseases. Based on a licensing agreement between MorphoSys and I-Mab signed in November 2017, I-Mab owns the exclusive rights for development and commercialization of MOR202/TJ202 in mainland China, Taiwan, Hong Kong and Macao.

Syndax Pharmaceuticals Announces Preclinical Profile and Initial Phase 1 Data
Demonstrating Clinical Activity of Menin Inhibitor SNDX-5613 in Adults with
Relapsed/Refractory Acute Leukemias

On April 27, 2020 Syndax Pharmaceuticals, Inc. ("Syndax," the "Company" or "we") (Nasdaq: SNDX), a clinical stage biopharmaceutical company developing an innovative pipeline of cancer therapies, reported that preclinical and initial clinical data for SNDX-5613, the Company’s potent, highly selective oral menin inhibitor (Press release, Syndax, APR 27, 2020, View Source [SID1234556630]). The oral presentation will be featured during the New Drugs on the Horizon session at the 2020 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Virtual Annual Meeting I. The New Drugs on the Horizon session will take place today at 4:50 p.m. ET and features discussions of innovative small molecules and biologics that have recently entered Phase 1 clinical trials.

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"Within months of initiating the Phase 1/2 AUGMENT-101 trial, we are excited to present to the cancer research community the first clinical evidence that disrupting the interaction between menin and MLL1 with our potent and selective inhibitor, SNDX-5613, can induce response in patients with genetically-defined acute leukemias," said Briggs W. Morrison, M.D., Chief Executive Officer of Syndax. "Notably, clinical activity was achieved rapidly after a single, 28-day cycle, a highly encouraging sign in this population of patients who face a particularly poor prognosis with few effective treatment options. We look forward to presenting additional findings from this trial in the fourth quarter."

The Company also announced today that SNDX-5613 was recently granted Orphan Drug Designation for the treatment of adult and pediatric acute myeloid leukemia (AML) by the U.S. Food and Drug Administration (FDA).

Preliminary AUGMENT-101

Data As of the April 17th data cutoff date, a total of six patients have been treated in the Phase 1 portion of the ongoing open-label AUGMENT-101 trial at increasing dose levels of SNDX-5613. Responses were observed in two of three patients harboring an MLL rearrangement. This included one patient, whose drug exposure was consistent with that needed for activity in preclinical models, who had a complete response with incomplete blood count recovery (CRi) after 28 days of therapy and subsequently improved to a complete response (CR). The second patient achieved a partial response with incomplete blood count recovery (PRi) after 28 days of therapy. Both patients continue to receive SNDX-5613. A third patient harboring an MLL rearrangement did not achieve drug exposure levels consistent with that needed for activity in preclinical models and was removed from the trial due to progressive disease. Treatment with SNDX-5613 has been tolerated well, with no dose limiting toxicities reported. One patient experienced a Grade 2 QTc prolongation but remains on treatment. Additional details regarding all six patients are available in the AACR (Free AACR Whitepaper) presentation.

"Three decades of scientific research exploring the menin-MLL-r interaction and its importance in this subset of leukemias have helped establish our confidence in the therapeutic potential of SNDX-5613 for leukemia patients harboring MLL-r and NPM1 mutations," said Jerry McGeehan, Ph.D., Vice President, Menin Program at Syndax Pharmaceuticals. "Following the recently published preclinical studies in Cancer Cell and Science magazine highlighting the activity of menin inhibition in genetically-defined leukemias, we are thrilled to demonstrate in the clinical setting that SNDX-5613 could serve as a targeted agent with the potential to deliver durable benefit to a severely underserved patient population."

The Company’s presentation also highlighted preclinical data supporting the potential of singleagent menin-MLL inhibition to serve as an effective intervention for both NPM1 mutant AML and MLL-r acute leukemias.

The AUGMENT-101 trial is a Phase 1/2 open-label trial designed to evaluate the safety, tolerability, pharmacokinetics and efficacy of orally administered SNDX-5613. The Phase 1 dose escalation portion of AUGMENT-101 was recently separated into two cohorts based on concomitant treatment with a strong CYP3A4 inhibitor. Arm A will enroll patients not receiving a strong CYP3A4 inhibitor, while Arm B will enroll patients receiving a strong CYP3A4 inhibitor. The Phase 1 dose escalation portion of AUGMENT-101 is currently enrolling adults with R/R acute leukemias including MLL-r and nucleophosmin (NPM1) mutant acute leukemias and is expected to establish a recommended Phase 2 dose for both cohorts by the fourth quarter of 2020. The Phase 2 portion will evaluate efficacy, as defined by CR rate (per International Working Group response criteria), across three expansion cohorts: MLL-r acute lymphoblastic leukemia (ALL), MLL-r AML and NPM1 mutant AML. MLL rearrangements are seen in 5-10% of AML and ALL, while NPM1 mutations are seen in 30% of adult AML cases. The Company expects to present additional results from AUGMENT-101 at a medical conference in the fourth quarter of 2020.

Additional AACR (Free AACR Whitepaper) Presentations

In addition to the SNDX-5613 presentation, data from the Phase 1 trials of the Company’s antiCSF-1R monoclonal antibody, axatilimab, both as a monotherapy and in combination with IMFINZI (durvalumab) in patients with locally-advanced or metastatic solid tumors, were summarized in two oral presentations. These data indicate that axatilimab is tolerated well in solid tumor patients, generated a recommended Phase 2 dose for axatilimab for the treatment of patients with solid tumors, and provided evidence of its ability to deplete circulating proinflammatory monocytes. A copy of all AACR (Free AACR Whitepaper) presentations will be available via Syndax’s website at View Source

About SNDX-5613

SNDX-5613 is a potent, selective, small molecule inhibitor of the menin-MLL binding interaction that is being developed for the treatment of MLL-rearranged (MLL-r) acute leukemias, including acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) and NPM1 mutant AML. In preclinical models of MLL-r acute leukemias, SNDX-5613 demonstrated robust, dosedependent inhibition of tumor growth, resulting in a marked survival benefit. Menin-MLL interaction inhibitors have also demonstrated robust treatment benefit in multiple preclinical models of NPM1 mutant AML, which represents the most frequent genetic abnormality in adult AML. SNDX-5613 is currently being evaluated in the Company’s AUGMENT-101 Phase 1/2 openlabel clinical trial for the treatment of relapsed/refractory (R/R) acute leukemias.

About Mixed Lineage Leukemia Rearranged (MLL-r)

Rearrangements of the MLL gene give rise to MLL-r acute leukemias, known to have a poor prognosis, with less than 55% of patients surviving past 5 years. MLL rearrangements produce fusion proteins that require interaction with the protein called menin to drive leukemic cancer growth. Disruption of the menin-MLL-r interaction has been shown to halt the growth of MLL-r leukemic cells. MLL-r leukemias, which are routinely diagnosed through currently available cytogenetic or molecular diagnostic techniques, occur in approximately 80% of infant acute leukemias and up to 10% of all acute leukemias. There are currently no approved therapies indicated for MLL-r leukemias.

About NPM1 Mutant Acute Myeloid Leukemia

NPM1 mutant AML, which is distinguished by point mutations in the NPM1 gene that drive the leukemic phenotype, is the most common type of cytogenetically normal adult AML and represents approximately 30% of all adult AML cases. This subtype of AML has a 5-year overall survival rate of approximately 50%. Similar to MLL-r leukemias, NPM1 mutant AML is highly dependent on the expression of specific developmental genes, shown to be negatively impacted by inhibitors of the menin-MLL interaction. NPM1 mutant AML is routinely diagnosed through currently available screening techniques. There are currently no approved therapies indicated for NPM1 mutant AML.

About Orphan Drug Designation

The Orphan Drug Designation program provides orphan status to drugs and biologics that are intended for the safe and effective treatment, diagnosis, or prevention of rare diseases that affect fewer than 200,000 people in the U.S. Among the benefits of orphan designation in the U.S. are seven years of market exclusivity following FDA approval, waiver or partial payment of application fees, and tax credits for clinical testing expenses conducted after orphan designation is received.

STAND UP TO CANCER FUNDED RESEARCH TO BE PRESENTED DURING THE AACR VIRTUAL MEETING 1 – APRIL 27-28, 2020

On April 27, 2020 Stand Up To Cancer (SU2C) reported that will be presented during the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual (AACR) (Free AACR Whitepaper) Virtual Meeting 10 from April 27th to 28th (Press release, Stand Up To Cancer, APR 27, 2020, View Source [SID1234556629]).

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Work presented by SU2C-funded investigators highlights continued support for developing effective immunotherapy approaches to pediatric and young adult ALL and lung cancer as well as progress in the emerging field of Cancer Interception. Cancer Interception seeks approaches to intervene and stop the formation or progression of early or pre-cancerous conditions.

"Stand Up To Cancer has invested significantly and has made notable contributions in advancing the field of immunotherapy and has pioneered new approaches to cancer diagnostics and treatment, notably through Cancer Interception," stated SU2C CEO Sung Poblete, PhD, RN. "Not only are we excited about the continuing impact SU2C is making in new immunotherapy approaches to treat refractory ALL in children and young adults and to treat non-small cell lung cancer, but we are making measurable strides in moving cancer interception forward toward clinical practice so we can treat patients at earlier stages to optimize patient outcomes.."

Tuesday, April 28, VMS.PR01.01. Translational Prevention Studies

10:50-11:00 a.m. (1098) – Mediators of early immune response in bronchial premalignant lesions

Members of the SU2C-LUNGevity Foundation-American Lung Association Lung Cancer Interception Dream Team used gene expression profiling to identify genes that may be responsible for immune suppression or activation in Bronchial premalignant lesions (PMLs) which are precursors to lung squamous cell carcinoma. Of 15 candidate genes identified, the GSTP1 gene was found to be upregulated in progressing lesions and negatively correlated with several immune activation pathways. Ultimately, GSTP1 represents a promising new target for immunotherapy of squamous cell lung cancer and may allow for novel early intervention treatments.
Tuesday, April 28, VCTPL05. Adoptive Cell Transfer Therapy

11:05-11:15 a.m. (CT051): Safety and efficacy of CD19/CD22 CAR T cells in children and young adults with relapsed/refractory ALL

Haneen Shalabi, DO, investigator on the St. Baldrick’s Foundation – Stand Up To Cancer Pediatric Cancer Dream Team reports that the team, which has been pioneering dual antigen targeting strategies for CAR T cell therapy, tested a novel humanized bispecific CD19/CD22 CAR T cell construct in patients with relapsed/refractory B ALL seeking to prevent antigen negative escape. In this phase 1 study, CD19/22 CAR was well tolerated and effective in CAR naïve patients, with four of six patients achieving minimal residual disease, negative complete remission. Future plans include exploring an additional dose level, intensifying lymphodepletion for prior CAR patients, and evaluating CAR T-cell product characteristics with outcomes.
1:00-1:10 p.m. (CT056): Durable complete responses to adoptive cell transfer using tumor infiltrating lymphocytes (TIL) in non-small cell lung cancer (NSCLC): a phase I trial.

Ben Creelan, MD, clinical lead on the SU2C Catalyst Lung Cancer Immunotherapy Research Team, led by Scott J. Antonia, MD, PhD, H. Lee Moffitt Cancer Center & Research Institute, will be presenting data on durable complete responses in metastatic non-small cell lung cancer (NSCLC) with manageable toxicity, potentially extending the benefits of adoptive cell transfer seen in melanoma to NSCLC.
Tuesday, April 28, VCTPL02. Early Detection and ctDNA

2:30-2:40 p.m. (CT023): Phylogenetic tracking and minimal residual disease detection using ctDNA in early-stage NSCLC: A lung TRACERx study

Christopher Abbosh, MB, young investigator on the SU2C-LUNGeivity-American Lung Association Lung Cancer Interception Dream Team reports that circulating tumor DNA is an adjuvant biomarker capable of both detecting minimal residual disease following surgery and defining the clonality of relapsing disease. These data pave the way for clinical trials predicated on escalation of adjuvant standard of care in patients who exhibit minimal residual disease following surgery.
Tuesday, April 28, VMS.CL11.01 – Predictive Biomarkers for Immunotherapeutics

3:55-4:05 p.m. (5666) – A noninvasive approach for early prediction of therapeutic benefit from immune checkpoint inhibition for lung cancer.

Maximilian Diehn, MD, PhD, co-leader and Ash Alizadeh, MD, investigator on the SU2C-LUNGevity Foundation-American Lung Association Lung Cancer Interception Research Team, and other team members report on the use of circulating tumor DNA to predict which non-small cell lung cancer (NSCLC) patients will achieve durable clinical benefit after treatment with immune checkpoint inhibitors. Currently, conventional imaging is often not able to identify which patients will achieve durable clinical benefit. The team was able to demonstrate that pre-treatment circulating tumor DNA and circulating immune profiles can provide accurate, noninvasive, and early forecasting of ultimate outcomes for NSCLC patients receiving immune checkpoint inhibitor therapy.

Erasca Raises $200 Million Series B Financing

On April 27, 2020 Erasca, a company whose mission is to erase cancer, reported the completion of a $200 million Series B financing round co-led by ARCH Venture Partners and Cormorant Asset Management (Press release, Erasca, APR 27, 2020, View Source [SID1234556627]). New investors participating in this financing include global Singapore-based investor EDBI, Invus, Terra Magnum Capital Partners and other private and strategic investors. Existing investors City Hill Ventures, Colt Ventures and LifeSci Venture Partners also participated meaningfully in the round.

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This financing brings the total capital raised by the company to more than $260 million. Erasca will use the proceeds to support the clinical development of multiple promising oncology programs and further advance the company’s in-house drug discovery pipeline.

"We are honored by the magnitude of support from such an impressive syndicate of investors, especially during these turbulent times," said Jonathan E. Lim, M.D., Erasca’s chairman, CEO and co-founder. "Unfortunately, millions of people still suffer from cancer daily. At Erasca, we are doing everything we can to help these patients live longer and healthier lives by taking an aggressive long-term approach to tackling this disease with leading-edge science and world-class talent. We are immensely grateful to have new and existing shareholders who embrace our mission to erase cancer."

Erasca has assembled a robust pipeline of targeted therapies directed at undisclosed targets through in-house drug discovery as well as active pipeline expansion through collaborations with world-class academic and biopharmaceutical organizations.

"We are pleased to continue backing Erasca’s terrific team and bold mission," said Kristina Burow, managing director at ARCH Venture Partners. "Cancer is a formidable disease. Therefore, Erasca’s team has built an impressive portfolio of potentially first-in-class and best-in-class assets, including successful in-licensing of several key programs to address significant unmet needs. The company has the talent, assets and perseverance to substantially change the trajectory of cancer treatment and improve patient outcomes in a meaningful way."

Bihua Chen, portfolio manager of Cormorant Asset Management, added, "Erasca continues to strengthen and build upon its exciting foundation. I have been impressed by how much progress the Erasca team has made since commencing operations just 18 months ago. I am confident that this team, now armed with an expanded portfolio and a bolstered balance sheet, will continue to execute on the pipeline and develop novel and impactful therapies for patients."

eFFECTOR’s Zotatifin (eFT226) Inhibited Tumor Growth and Caused Tumor Regression Across Diverse Receptor Tyrosine Kinase-Driven Tumor Types in Preclinical Models of Disease

On April 27, 2020 eFFECTOR Therapeutics, Inc., a leader in the development of selective translation regulator inhibitors (STRIs) for the treatment of cancer, reported that data presented today in a virtual session at the AACR (Free AACR Whitepaper) Annual Meeting, showed the anti-tumor activity of the company’s product candidate, zotatifin, in preclinical models of FGFR1, FGFR2 and HER2 driven cancers, demonstrating the potential of zotatifin in receptor tyrosine kinase (RTK)-driven cancers (Press release, eFFECTOR Therapeutics, APR 27, 2020, View Source [SID1234556626]).

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Peggy A. Thompson, Ph.D., executive director, translational medicine at eFFECTOR, gave a presentation entitled, "Preclinical evaluation of eFT226, a potent and selective eIF4A inhibitor with anti-tumor activity in FGFR1, FGFR2 and HER2 driven cancers" which showed that zotatifin significantly inhibited tumor growth and caused tumor regression across diverse RTK-driven tumor types. Zotatifin has been shown to downregulate RTK protein levels and associated AKT and MAPK signaling, resulting in anti-tumor activity in FGFR1, FGFR2 and HER2 driven models. In a HER2+ breast cancer model, tumor regression was sustained long after cessation of therapy. Further evaluation of predictive markers of sensitivity or resistance showed that RTK tumor models with mTOR mediated activation of eIF4A are most sensitive to zotatifin.

"These promising preclinical studies demonstrated that the association of zotatifin activity in RTK tumor models with mTOR pathway activation provides an opportunity to further enrich for sensitive patient subsets during clinical development," said Steve Worland, Ph.D., president and chief executive officer of eFFECTOR. "This selection strategy will complement our selection of KRAS-mutant tumors based on zotatifin’s down-regulation of KRAS protein in preclinical studies."

A Phase 1/2 clinical trial of zotatifin in patients with KRAS- or RTK-mutant solid tumors is ongoing [NCT04092673]. The trial is enrolling patients with activating mutations, amplifications or fusions in HER2, ERBB3, FGFR1, or FGFR2 receptor tyrosine kinases, or any KRAS mutation subtype. The primary objectives of the trial include safety and tolerability of zotatifin as monotherapy. Secondary objectives include antitumor activity and survival, as well as pharmacokinetics of the drug. Exploratory objectives include pharmacodynamics of zotatifin.

About Zotatifin
Zotatifin is a potent and sequence selective inhibitor of eukaryotic translation initiation factor 4A (eIF4A) mediated translation. Zotatifin is designed to inhibit the translation of mRNAs encoding several important oncogenes and survival factors, including several RTKS, KRAS, Cyclin D, CDK4/6, MYC, MCL1 and BCL-2 resulting in potent in vivo tumor regression in multiple tumor models dependent on these factors, including colorectal cancer, non-small cell lung cancer, breast cancer, hepatocellular carcinoma and B cell lymphomas. Since zotatifin inhibits the translation of mRNA encoding KRAS and RTK, it is not limited to any mutation subtypes. The product candidate is currently being evaluated in a Phase 1/2 clinical trial in patients with solid tumors.

About eIF4A
eIF4A is an RNA helicase that catalyzes the ATP-dependent translation of highly structured mRNA. eIF4A helicase activity is tightly controlled by the PI3K and RAS signaling pathways. Activation of eIF4A results in the selective upregulation of oncogenes with highly structured 5’-UTRs (untranslated regions) that are involved in cell proliferation, survival and metastasis. Inhibition of eIF4A selectively regulates the translation of a set of target mRNAs distinct from those regulated by MNK1/2 and eIF4E. Targeting these selective translational regulators may expand the potential patient population that benefits from translation regulation therapy.