News Careers Contact About Science Pipeline Patients Investors SCIENCE eFFECTOR is pioneering the field of Selective Translation Regulator Inhibitors (STRIs). Transcription is the copying of DNA sequences into mRNA, whereas translation is the subsequent utilization of mRNA sequences to direct protein synthesis. eFFECTOR’s translation regulation targets are at a key node where oncogenic signaling pathways converge to impact multiple complementary cancer growth and survival mechanisms. The importance of translation regulation in disease is becoming increasingly recognized in the pharmaceutical industry, and we believe we are at the forefront of developing novel approaches to cancer therapy focused on STRIs. Utilizing our proprietary selective translation regulation technology platform and expertise, we have developed an understanding of genes that are translationally upregulated in multiple tumor types. This has enabled us to identify specific points of therapeutic intervention that may have a meaningful clinical effect. OUR PROGRAMS Our programs target three distinct targets central to the eIF4F translation initiation complex: MNK, eIF4A and eIF4E. Each of these targets regulates distinct sets of genes in cancer and immune cells. MNK eIF4A eIF4E The eIF4F Complex The eIF4F complex plays a critical role in the production of certain proteins that promote cell growth, division and survival. eIF4F is a central junction where two of the most frequently activated signaling pathways in cancer, the PI3K-AKT and RAS-MEK pathways, converge. It is a central node that initiates the translation of the proteins that are frequent culprits in key disease-driving processes. Activation of growth signaling pathways such as receptor tyrosine kinase (RTK) pathways, along with downstream PI3K-AKT and RAS-MEK pathways, converges on eIF4F and initiates over-production of multiple pro-growth proteins. Especially high activation of these growth signaling pathways can cause eIF4F activation that is excessive and continuous, resulting in upregulation of protein synthesis. This upregulation leads to uncontrolled growth of tumor cells, as well as exhaustion of T cells – causing T cells to become less effective cancer fighters. eIF4F complex controls production of multiple cancer driving proteins simultaneously MNK eIF4A eIF4G eIF4E eIF4F COMPLEX Next PUBLICATIONS & PRESENTATIONS Dissection of cancer therapy combinations in RTK driven tumors using Zotatifin (eFT226), a potent and selective elF4A inhibitor 2020 EORTC-NCI-AACR 32nd Symposium Download Selection of Zotatifin(eFT226) combination partners based on translational regulation of target oncogenes 2020 CSHL Translational Control Meeting Download A Phase II, Open-Label Study Of Tomivosertib (eFT508) Added On To Continued Checkpoint Inhibitor Therapy In Patients With Insufficient Response To Single Agent Treatment 2020 American Society of Clinical Oncology (ASCO) Annual Meeting Download eFT226, a first in class inhibitor of eIF4A, targets FGFR1/2 and HER2 driven cancers AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics 2019 Download Physical and Functional Interactions between MNK and mTOR Signaling Regulate the Activation and Differentiation of T Cells American Association for Cancer Research (AACR) Annual Meeting 2019 Download A focused CRISPR screen to identify synthetic lethal interactions with the novel eIF4A Inhibitor eFT226 in KRAS driven NSCLC American Association for Cancer Research (AACR) Annual Meeting 2019 Download Targeting Hormone Receptor-Dependent Cancers with Potent, Selective and Orally-Available Small Molecule Inhibitors of eIF4E American Association for Cancer Research (AACR) Annual Meeting 2019 Download Tomivosertib (eFT508), a Potent and Highly Selective Inhibitor of MNK1 and MNK2, Enhances CAR T Cell Activity Through Modulating T Cell Differentiation American Association for Cancer Research (AACR) Annual Meeting 2019 Download Targeting PI3K/mTOR Signaling with Potent, Selective and Orally-Available Small Molecule Inhibitors of eIF4E AACR Special Conference 2018 Download Inhibition of MNK by eFT508 reprograms T-cell signaling to promote an anti-tumor immune response AACR Annual Meeting 2018 Download eFT508, A Potent and Highly Selective Inhibitor of MNK 1/2, Regulates T Cell Differentiation Promoting an Anti-tumor Immune Response AACR Annual Meeting 2018 Download A Phase 1-2 Dose-Escalation and Cohort-Expansion Study of eFT508, a Selective, Orally Bioavailable Inhibitor of MNK1 and MNK2, in Patients with Hematological Malignancies American Society of Hematology (ASH) Annual Meeting 2017 Download Preclinical Evaluation of eFT226, a Novel, Potent and Selective elF4A Inhibitor with Anti-tumor Activity in B-cell Malignancies American Society of Hematology (ASH) Annual Meeting 2017 Download eFT508, A Potent and Highly Selective Inhibitor of MNK 1 and MNK2, is an Activator of Anti-Tumor Immune Response 2017 Society for Immunotherapy of Cancer (SITC) 32nd Annual Meeting Download A Phase 1 Dose Escalation Study of eFT508, an Inhibitor of Mitogen-Activated Protein Kinase-Interacting Serine/Threonine Kinase-1 (MNK-1) and MNK-2 in Patients with Advanced Solid Tumors 2017 American Society of Clinical Oncology (ASCO) Annual Meeting Download eFT508, A Potent and Highly Selective Inhibitor of MNK 1/2, Regulates Immune Checkpoint and Cytokine Expression Promoting Anti-tumor Immunity American Association for Cancer Research (AACR) Annual Meeting 2017 Download eFT508, a Potent and Selective Mitogen-Activated Protein Kinase Interacting Kinase (MNK) 1 and 2 Inhibitor, is Efficacious in Preclinical Models of Diffuse Large B-Cell Lymphoma (DLBCL) American Society of Hematology (ASH) Annual Meeting 2015 Download About Science Pipeline Patients Investors News Careers Contact Copyright © 2021 eFFECTOR Therapeutics, Inc. | Privacy Policy