Antineoplastic Agents TRIZ Cases

Blocking GLUT5, KHK, FASN, and PI3K pathways limits fructose-driven colorectal and small intestine tumor growth and delays onset.

A multi-antibody serology panel improves non-invasive EBV-positive gastric cancer detection and risk stratification from biological samples.

Combining HDAC6 and GSK3β inhibitors blocks epithelial-mesenchymal transition to reduce cancer cell invasiveness and metastasis.

A brain-penetrant EGFR inhibitor addresses osimertinib-resistant NSCLC by targeting EGFR alterations and improving CNS metastasis control.

Embryonic zebrafish screening captures vertebrate phenotypes and helps prioritize compounds with better clinical relevance for cancer and other diseases.

Co-administering KRAS G12C and PARP inhibitors improves potency across resistant cancer cell lines and raises therapeutic benefit.

Dual-target CD19/22 CAR T-cells address CD19-negative relapse and weak CD22 synapse formation to improve persistence in pediatric B-ALL.

A combined Cimicifuga and Petasites extract improves anticancer efficacy through synergistic action while supporting safer therapeutic and prophylactic use.

Targeting Wnt signaling and DNA repair together helps treat resistant pancreatic, ovarian, and cholangio-carcinomas with lower inhibitor doses.

Engineered T cells pair a PVR-binding CAR with FRα×CD3ε BiTE secretion to overcome FRα heterogeneity and kill broader tumor cell populations.

Combining ROCK and OXPHOS inhibitors counters rapid cancer-cell adaptation, inducing energetic stress and strong tumor inhibition with minimal toxicity.

Combined metabolism-modulating agents target resistant cancer stem cells through multiple pathways to induce cell death and reduce relapse risk.

Blocking ATG4B-mediated autophagy helps glioblastoma resist less, making radiation, alkylating agents, and mTOR inhibitors more cytotoxic.

Flexible vodobatinib dosing helps manage CML and Ph+ ALL despite BCR-ABL1 mutations while limiting severe adverse events.

Combining a 4-aminoisoindoline-1,3-dione compound with targeted agents helps overcome resistance and limit side effects in blood cancers.

Combining PARP, DNA repair, and epigenetic inhibitors enables lower-dose treatment of H3 mutant cancers while reducing side effects and recurrence.

Combining a BCL-2/BCL-XL inhibitor with homoharringtonine helps overcome resistance in hematologic cancers by driving apoptosis.

Oral satraplatin addresses PCNSL treatment limits by crossing the blood-brain barrier while reducing cisplatin-like toxicity.

Combining CDK7 inhibitors with checkpoint, PARP, or cytotoxic agents boosts anti-tumor efficacy and restores sensitivity in resistant cancer cells.

Targeting upregulated FN14 with an FN14 inhibitor plus a kinase inhibitor suppresses TWEAK/FN14 signaling and reduces tumor growth.

Combining PI3K, CDK4/6, and endocrine therapies helps delay resistance and improve tumor regression in HR+/HER2− breast cancer.

Combined metabolism modulators target resistant cancer stem cells by disrupting survival pathways to induce cell death and reduce relapse risk.

Blocking DNA-PK with an imidazolinone derivative helps overcome tumor DNA repair during radiotherapy, improving anti-tumor response.

1,3,5-triazine derivatives inhibit endosomal trafficking and autophagy to kill resistant cancer cells and reshape macrophage-driven tumor microenvironments.