Two-target antibody drugs to close the antigen escape route
If a drug relies on one marker, the tumour can survive by dropping it. A drug that recognises two markers at once makes that escape harder.
Bispecific ADCs binding two tumour antigens can retain binding and internalisation when one antigen is lost, and may improve selectivity where either antigen alone is present on normal tissue. Several bispecific ADCs are in clinical development. The proposal is to test the antigen-escape hypothesis explicitly by comparing a bispecific ADC with its monospecific parent and measuring antigen status at progression.
- Acquired resistance to every therapy · Nearly every targeted therapy stops working within months to a few years as the tumour adapts.
- Tumour heterogeneity and clonal evolution · A tumour is many tumours. Treatments that kill most cells leave the rest to grow back, changed.
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not linked directly; found by shared links- PersonLi Zhang
Shares SystImmune / Sichuan Biokin, Izalontamab brengitecan.
- TrialPANKU-Esophagus01 (BL-B01D1-305)
Shares Izalontamab brengitecan, Bispecific ADC.
- ProductTrastuzumab brengitecan
Shares SystImmune / Sichuan Biokin, Antibody-drug conjugate (ADC).
- TrialBL-B01D1-307
Shares Izalontamab brengitecan, Bispecific ADC.
- IdeaSlow the tumour's mutation engine with APOBEC inhibitors during targeted therapy
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy.
- IdeaSwitch drugs at maximum response, not at relapse
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy.
- TermHydrophilic next-generation linkers (TMALIN, Dolaflexin, sulfonyl-pyrimidine, PEG-containing)
Shares Izalontamab brengitecan, Antibody-drug conjugate (ADC).
- IdeaAn open atlas of collateral sensitivity for every approved targeted drug
Shares Tumour heterogeneity and clonal evolution, Acquired resistance to every therapy.