Antibody Ingredients TRIZ Cases

Combining anti-αvβ3 and anti-PD-1 antibodies helps overcome primary resistance by blocking angiogenesis and boosting tumor inhibition.

By binding tumor-cell MICA/B, these antibodies block proteolytic shedding and restore NKG2D-dependent NK and T cell activation.

Engineered CD28 antibodies preserve T cell co-stimulation while avoiding super-agonistic cytokine release and adding CTLA-4 checkpoint inhibition.

Delayed PD-1 axis blockade 3-5 weeks after MAGE-A4-targeted T-cell infusion helps sustain anti-tumour activity and limit exhaustion.

Combining tebentafusp with PD(L)1 or CTLA-4 inhibitors recruits CD8+ T cells to resistant melanoma and improves tumor response.

Targeting membrane-bound ER-α36 with lasofoxifene helps suppress tamoxifen-resistant tumor growth and supports combination treatment strategies.

Preoperative PD-L1 inhibitor therapy helps reduce viable tumor cells before resection of gastric, esophageal, and liver cancers with good tolerability.

A knobs-in-holes bispecific antibody pairs IL-6Rα and IL-8R targeting in one molecule to block metastasis without combination dosing complexity.

Combining anti-CD19 antibodies with natural killer cells boosts ADCC and improves killing of B-cell tumors with synergistic effects.

Bispecific anti-Vβ17 antibodies redirect Vβ17+ T cells to tumor antigens, boosting activation markers and killing cancer cells.

CDCP1-binding antibodies deliver cytotoxic payloads into tumor cells to improve anti-cancer efficacy while reducing non-specific toxicity.

Engineered anti-CCR8 antibodies overcome weak GPCR binding by targeting intact CCR8, enabling signaling blockade, ADCC, and primate cross-reactivity.

By blocking TFPI Kunitz domains, this antibody restores coagulation in hemophilia while reducing frequent infusions and bleeding events.

Targeted CDR sequence changes improve IL-11Rα binding, signaling inhibition, and glycosylation homogeneity for therapeutic antibody development.

Low-pH buffers, saccharides, and surfactants keep T cell engaging antibody constructs stable at high concentration by reducing aggregation.

Targeting CAPRIN-1 with a benzodiazepine-linked antibody conjugate strengthens antitumor effects across multiple cancer types.

Selective anti-MSLN antibodies avoid soluble mesothelin sink effects, prolong tumor binding, and improve ADCC at tumor cells.

Tumor-reactive haptens create cell-surface neoantigens that engineered antibodies detect without MHC allele restriction, reducing off-tumor toxicity.

Blocking SIRPα-CD47 with an Fc-silenced IgG4 antibody boosts tumor phagocytosis while minimizing self-attack on immune cells.

Combining anti-fucosyl-GM1 with anti-CD137 boosts NK cell CD137 signaling at tumors while lowering systemic immune stimulation and dose.

Selective EMR2 and TRBV19 binding targets AML and MDS cells while limiting broad T-cell activation, cytokine release syndrome, and healthy-cell toxicity.

Combining anti-TROP2 or anti-HER2 ADCs with bispecific checkpoint inhibitors boosts antitumor durability while helping manage toxicity.

Highly specific CEACAM5 antibodies use engineered CDR sequences to avoid CEACAM cross-reactivity and improve targeted cancer cell killing.

A bispecific binder targets CD39 and CD73 to inhibit ATP-ADO signaling, trigger CD73 endocytosis, and reduce tumor immune escape.

By splitting IL12 receptor activation into tumor-targeted β1 and β2 agonists, this case improves anti-tumor activity while reducing systemic toxicity.

Combining ADCC-enhanced anti-CD19 antibody therapy with γδ T-cells increases tumor cell lysis in leukemia and lymphoma samples.

By disrupting allelic exclusion in rodents, engineered immunoglobulin alleles enable faster bispecific antibody production with broader diversity.

Engineered tyrosine residues enable fast, site-specific ADC conjugation with higher DAR, improved homogeneity, and no deglycosylation step.

A humanized anti-BCMA antibody uses optimized CDRs to improve affinity, endocytosis, thermal stability, and monkey cross-reactivity.

Dual-target antibody molecules block CD96 and TIGIT interactions to boost T cell and NK cell activity in immune-suppressed disease settings.

Variable-domain mutations tune ipilimumab to bind CTLA-4 more strongly in acidic tumors, improving anti-tumor activity while limiting toxicity.

Multispecific DLL3-binding antibodies recruit T cells to kill DLL3-positive tumors while reducing cytokine-related side effects.

A 3E10-based bispecific scFv enters cells through hENT2 and binds intracellular Mdm2, enabling specific inhibition with low toxicity.

A single antibody combines PD1 antagonism with VEGFR2 blockade to extend treatment durability and avoid the added toxicity of separate agents.

Combining anti-CD19 ADCs with anti-CD79b agents improves efficacy in refractory CD19+ cancers while reducing systemic toxicity.

Engineered anti-IgE fragments release cell-bound IgE from FcεRI without triggering immune cells, while improving thermal and chemical stability.

A dual-binding macromolecule localizes therapy through an address target before effector binding, improving specificity while limiting off-target effects.

By targeting the ACE2 receptor instead of variable spike proteins, these antibodies block diverse SARS-related coronaviruses without disrupting ACE2 activity.

Engineered IgE-binding antibodies release cell-bound IgE from FcεRI without activating basophils or mast cells, while improving stability.

Specific anti-CD84 CDR sequences improve tumor microenvironment targeting while driving apoptosis and lowering tumor burden in leukemia models.

High-affinity anti-OX40 antibodies are engineered to block T cell proliferation without residual agonism or excess Treg depletion.

Low-volume anti-OX40L injections extend dosing intervals in atopic dermatitis while maintaining efficacy and reducing needle burden.

Targeted heavy-chain substitutions at AHo positions 56 and 80 raise monoclonal antibody titer, purity, and thermal stability.

Engineered heavy-chain asymmetry and staged purification improve bispecific B7H3-GD2 antibody yield, pairing fidelity, and purity.

Anti-transferrin receptor conjugates deliver siRNA or ASOs to cardiac muscle cells to suppress PLN mRNA and address mutation-driven cardiomyopathy.

Engineered anti-CD47 and CD19/CD47 antibodies block CD47-SIRPα while reducing toxicity and improving pharmacokinetics in cancer treatment.

High-affinity tetravalent EPOR antibodies stimulate erythropoiesis to treat anemia while limiting harmful non-erythropoietic signaling.

Selective anti-ACTH antibodies bind the central ACTH region to lower cortisol and aldosterone while avoiding hyperpigmentation.