EGFR (Epidermal growth factor receptor)

P=N/A, N=100, Not yet recruiting, AstraZeneca

P3, N=98, Active, not recruiting, AstraZeneca | Trial completion date: Jun 2026 --> Jun 2027

P2, N=40, Recruiting, Fudan University | Not yet recruiting --> Recruiting

The HER2 inhibitors represent different mechanisms of actions, including trastuzumab, pertuzumab, tucatinib, and lapatinib, all of which are clinically approved, as well as PEPDG278D, a recombinant human protein which was previously shown to induce the degradation of HER2 and epidermal growth factor receptor (EGFR). Despite p95HER2 expression and resistance to current HER2 inhibitors, HER2-positive BC cells and tumors are highly vulnerable to PEPDG278D-induced degradation of HER2 and EGFR. By inducing HER2 degradation, PEPDG278D eliminates p95HER2 in HER2-positive BC cells and tumors.

Mechanistically, galangin suppressed M2 macrophage polarization, directly interacted with the efferocytosis-related targets CAMK2A and MERTK, and reduced their expression. Together, these findings establish efferocytosis as a novel and targetable vulnerability in drug-resistant NSCLC and highlight galangin as a promising sensitizer for overcoming resistance to two major targeted therapies.

The limitations of oxycodone in chronic neuropathic and bone metastasis pain are discussed, alongside recent advances in oxycodone formulation development and novel analgesics in China. Individualized treatment strategies integrating pharmacogenomic profiles and multimodal approaches are encouraged.

Functional perturbation studies further indicated that EGFR, TNFα, and TNFAIP3 contribute to PTOX-induced macrophage clearance. Together, these findings identify PTOX as a novel phagocytosis-sensitizing agent and support its potential as a combinatorial immunotherapeutic strategy to enhance CD47-targeted therapy in TNBC.

BISDA displayed 48-h IC50 of 2.609 µg mL-1 in A549 cells, decreased viability compared to controls, and was less toxic than cisplatin while inducing apoptosis, G2/M cell cycle arrest, and inhibiting cancer cell migration...Principal component analysis showed that BISDA reprogrammed signaling through decoupling of the EGFR-mTOR axis from the TGFβ-AKT1-MAPK3-HSP90 cluster, indicative of a global rewiring of pathways. These results suggest that BISDA may serve as a multifaceted inhibitor for treating LUAD, acting in an antiproliferative capacity through apoptosis induction while also preventing signaling pathways associated with resistance.

According to transcriptome analysis, CDCA-Ver mainly activated "Metabolic pathways" and "Cell cycle" targets. This study could provide scientific basis for the application of CDCA-Ver.

RMSD and RMSF analyses revealed that naringin, the major compound of I. aschersoniana, exhibited dynamically stable binding within the active sites of AKT1, EGFR, and PPARG proteins, with AKT1@Naringin and PPARG@Naringin complexes displaying a more stable dynamic profile. In this network pharmacology study, forty-five common targets between the major compounds of I. aschersoniana with breast and colon cancers were identified.

A previous analysis of the RELAY phase 3 liquid biopsy addendum demonstrated suppressed EGFR-activating mutation allele count, increased total cell-free DNA (cfDNA) concentration, and shortened cfDNA fragment size with ramucirumab (RAM) plus erlotinib (ERL) versus placebo (PL) plus ERL in patients with EGFR-mutated NSCLC. This updated analysis revealed differences in total cfDNA concentration and T790M mutation rates between ex19del and L858R. RAM plus ERL may exhibit greater antitumor effects on L858R, supporting the favorable survival benefits observed previously in patients with a L858R.

The sequential multibiomarker algorithm achieved 96.5% sensitivity and 98.7% specificity for malignant PE detection, with 85.3% overall three-way classification accuracy. Multiomics integration combining proteomic biomarkers with single-cell immune profiling and genomic mutation characterization achieves high diagnostic accuracy for pleural effusion while revealing disease-specific immune mechanisms and mutation-driven therapeutic opportunities.