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- | Journal: ERK1/2 mitogen-activated protein kinase dimerization is essential for the regulation of cell motility. (Pubmed Central) - Sep 12, 2024
In agreement, clinical data disclose that high KSR1 expression levels correlate with greater metastatic potential and adverse evolution of mammary tumors. Overall, our results portray both ERK dimerization and KSR1 as essential factors for the regulation of cell motility and mammary tumor dissemination.
- | DEL-22379 / IBBTEC, Vichem
Journal: Inhibiting ERK dimerization ameliorates BRAF-driven anaplastic thyroid cancer. (Pubmed Central) - Sep 10, 2022
Nonetheless, DEL-22379 demonstrated significant anti-tumor effects against BRAF-mutant cells in vivo with an apparent lack of toxicity, making it an interesting candidate for the development of combinatorial treatments. Our data underscore the differences elicited by the specific driver mutation for thyroid cancer onset and progression, which should be considered for experimental and clinical approaches.
- || DEL-22379 / IBBTEC, Vichem
Clinical, Journal: Structure-activity relationship study of DEL-22379: ERK dimerization inhibitors with increased safety. (Pubmed Central) - Nov 24, 2021
The structure-activity relationship of idolin-2-one scaffold and the impact of Z/E configuration on potency were discussed. Potential safety of two synthesized analogues was investigated and in silico docking study of five compounds was performed to understand the structural basis of ERK dimerization inhibition.
- [VIRTUAL] ERK dimerization promotes migration and invasion () - May 30, 2021 - Abstract #EACR2021EACR_2595;
Blocking ERK dimers formation reduced invasion capacity of MCF-7 and MDA-231-MB tumors cells. Thus, targeting ERK dimerization could emerge as a valid therapeutic strategy for the treatment of breast cancer.
- [VIRTUAL] ERK dimerization promotes migration and invasion () - May 30, 2021 - Abstract #EACR2021EACR_2594;
Blocking ERK dimers formation reduced invasion capacity of MCF-7 and MDA-231-MB tumors cells. Thus, targeting ERK dimerization could emerge as a valid therapeutic strategy for the treatment of breast cancer.
- [VIRTUAL] ERK dimerization promotes migration and invasion () - May 30, 2021 - Abstract #EACR2021EACR_2593;
Blocking ERK dimers formation reduced invasion capacity of MCF-7 and MDA-231-MB tumors cells. Thus, targeting ERK dimerization could emerge as a valid therapeutic strategy for the treatment of breast cancer.
- [VIRTUAL] ERK dimerization promotes migration and invasion () - May 30, 2021 - Abstract #EACR2021EACR_2592;
Blocking ERK dimers formation reduced invasion capacity of MCF-7 and MDA-231-MB tumors cells. Thus, targeting ERK dimerization could emerge as a valid therapeutic strategy for the treatment of breast cancer.
- | Journal: Two Targets, One Hit: new Anticancer Therapeutics to Prevent Tumorigenesis Without Cardiotoxicity. (Pubmed Central) - Mar 2, 2021
The promising new field of cardio-oncology offers the identification of potent anti-cancer therapeutics that effectively inhibit cancer cell proliferation without causing cardiotoxicity. Future introduction of recently identified cardio-safe compounds into clinical practice (including ERK dimerization inhibitors or BAX allosteric inhibitors) is expected to help oncologists avoid unwanted cardiological complications associated with therapeutic interventions.
- [VIRTUAL] Combined JAK2 and ERK1 / 2 kinase inhibition as a new therapeutic approach for myeloproliferative neoplasias (Abstract video presentations) - Sep 3, 2020 - Abstract #DGHO2020DGHO_1947;
We assessed ERK inhibitors interfering with ATP binding (LTT462, MK8353) or ERK dimerization (DEL22379) as single agents and in combination with the JAK2 inhibitor ruxolitinib. Our data demonstrate that dual inhibition of JAK2 and ERK1/2 enhances the corrective potential in MPN indicating that ERK kinases should be targeted to increase therapeutic efficacy.
- [VIRTUAL] Combined JAK2 and ERK1 / 2 kinase inhibition as a new therapeutic approach for myeloproliferative neoplasias (Abstract video presentations) - Sep 3, 2020 - Abstract #DGHO2020DGHO_1314;
We assessed ERK inhibitors interfering with ATP binding (LTT462, MK8353) or ERK dimerization (DEL22379) as single agents and in combination with the JAK2 inhibitor ruxolitinib. Our data demonstrate that dual inhibition of JAK2 and ERK1/2 enhances the corrective potential in MPN indicating that ERK kinases should be targeted to increase therapeutic efficacy.
- [VIRTUAL] Combined JAK2 and ERK1 / 2 kinase inhibition as a new therapeutic approach for myeloproliferative neoplasias (Nairobi) - Sep 3, 2020 - Abstract #DGHO2020DGHO_920;
We assessed ERK inhibitors interfering with ATP binding (LTT462, MK8353) or ERK dimerization (DEL22379) as single agents and in combination with the JAK2 inhibitor ruxolitinib. Our data demonstrate that dual inhibition of JAK2 and ERK1/2 enhances the corrective potential in MPN indicating that ERK kinases should be targeted to increase therapeutic efficacy.
- [VIRTUAL] Combined JAK2 and ERK1 / 2 kinase inhibition as a new therapeutic approach for myeloproliferative neoplasias (Abstract video presentations) - Sep 3, 2020 - Abstract #DGHO2020DGHO_555;
We assessed ERK inhibitors interfering with ATP binding (LTT462, MK8353) or ERK dimerization (DEL22379) as single agents and in combination with the JAK2 inhibitor ruxolitinib. Our data demonstrate that dual inhibition of JAK2 and ERK1/2 enhances the corrective potential in MPN indicating that ERK kinases should be targeted to increase therapeutic efficacy.
- ||| Journal, Adverse events: Interference with ERK-dimerization at the nucleocytosolic interface targets pathological ERK1/2 signaling without cardiotoxic side-effects. (Pubmed Central) - Jul 24, 2020
We also examine this alternative ERK1/2-targeting strategy in cancer: indeed, ERK-phosphorylation is strongly upregulated in cancer and EDI efficiently suppresses cancer cell proliferation without causing cardiotoxicity. This powerful cardio-safe strategy of interfering with ERK-dimerization thus combats pathological ERK1/2-signaling in heart and cancer, and may potentially expand therapeutic options for ERK1/2-related diseases, such as heart failure and genetic syndromes.