Antibody Ingredients TRIZ Cases

This case combines YTHDF2 inhibitors with PD-1 or PD-L1 blockade to counter TAM immunosuppression and support CD8+ T cells.

This case combines PI3K inhibitors with checkpoint inhibitors to induce MHC II expression and improve GBM immune targeting.

This case combines HLA-G, EGFR, PD-1/PD-L1, and CD47/SIRPα antibodies to enhance phagocytosis, T-cell activity, and tumor regression.

Humanized antibodies and CAR T cells bind B7S1, block its inhibition, and enhance immune activation against cancer cells.

Engineered anti-FGFR2b antibodies block KGF binding and deliver cytotoxic payloads with reduced corneal and systemic toxicity.

This case uses defined heavy- and light-chain CDRs to strengthen PVRIG binding and support checkpoint inhibitor combinations.

This case uses anti-NPR1 antibodies to bypass neprilysin inhibition, activate cGMP signaling, and address heart failure and hypertension.

This case uses dual CD28 and CD22 binding to direct T-cell killing while limiting systemic cytokine storm.

Explore FcRn antibody variants that preserve affinity and biological activity while reducing aggregation through localized sequence changes.

This case uses sequence-defined fully human anti-PD-L1 antibodies to block PD-1 binding, enhance T-cell function, and simplify treatment.

Engineered c-Met ADCs use cysteine handles for controlled drug delivery.

An Fc-binding unit enables site-specific conjugation while preserving antibody function.

This case uses engineered anti-PVRIG antibodies and bispecific formats to improve PVRIG-CD112 blockade and inhibit tumor proliferation.

This case uses localized CDR-H3 and CDR-L3 changes to improve CTLA-4 binding, block signaling, and activate immune attack.

This case shows how selective CD200R1 binding and affinity maturation enhance immune activation while limiting off-target effects.

Anti-TCRβV antibodies activate selected T cell subsets to support tumor cell lysis while reducing cytokine-related neurotoxicity.

This case uses epitope-specific anti-ACTH antibodies to block receptor signaling and limit cortisol and aldosterone secretion.

This case uses Fc-optimized CCR8 antibodies to block CCL1/CCR8, deplete tumor Tregs, and support anti-PD-1 therapy.

Targeted amino acid substitutions prevent immunogenic glycans while preserving antibody potency.

Multispecific TCRβV-targeting molecules focus T-cell activation, supporting tumor lysis while reducing cytokine storms and neurotoxicity.

This case uses IL17F supplementation or blockade to balance infection clearance with reduced organ dysfunction in sepsis.

Masked anti-EGFR antibodies activate at target sites to limit off-target toxicity.

CD68, CD8, CD20, CD163, and PD-L1 profiling guides immunotherapy selection for more consistent patient response.

This case uses anti-Siglec-9 antibodies to block sialic acid signaling and enhance NK cell cytotoxicity against cancer cells.

This case combines TfR targeting with PD1 binding to internalize complexes, deplete surface PD1, and sustain immune activation.

This case combines HER2 targeting with 4-1BB activation to extend cancer immunotherapy to low-HER2 tumors and limit liver toxicity.

This case combines CD28 and OX40 blockade in one antibody to curb effector T-cell proliferation and autoimmune signaling.

Anti-TIM-3 combinations strengthen antitumor immunity while reducing toxicity.

This case uses monoclonal antibodies against Gal3 CRD to inhibit interactions while avoiding cross-reactivity with Gal1 and Gal7.

This case examines a bispecific molecule that bridges myeloma cells and T cells to address resistance and treatment side effects.

ARD107 anti-CSPG4 antibodies link cytotoxic agents to CSPG4+ tumors, helping reduce cancer cells while sparing normal tissues.

This combination pairs HER2/neu targeting with PD-1 checkpoint inhibition to enhance ADCC and immune activity in low-expression cancers.

This case uses masking, cleavage, and temporary half-life extension to activate multispecific proteins at the target site.

A humanized anti-SEZ6 antibody linked to calicheamicin targets tumor-initiating cells, suppressing growth while reducing off-site toxicity.

This case pairs CAPRIN-1 targeting with sorafenib to raise phagocytic activity against cancer cells by about 2.3 times.

This case refines antibody CDRs and structure to improve CD25 affinity, Treg depletion, pharmacokinetics, and effector T-cell activity.

This case uses dual PSMA and CD3 binding to focus T-cell activation on tumor cells rather than direct toxic damage.

This case targets ILT4 epitopes to block HLA-G signaling and improve T-cell therapy response in myeloid-rich tumors.

This case combines PD-L1 binding with constant-domain CD137 recognition to localize immune activation and reduce liver toxicity.

The case combines CD38 activity modulation, immune-cell proliferation, and ADCC to address limited solid-tumor targeting.

This case develops LAG-3 antibodies with optimized binding to block immune suppression and support T-cell activation.

This case modifies antibody CDR regions to reduce HLA binding and immune responses while preserving CD3 targeting and limiting toxicity.

This combination boosts ADCC and CDC in CD20-expressing cancers, addressing weak synergy between standard antibody and BTK treatment.

Novel antibodies bind human CD73 at specific epitopes to inhibit enzymatic activity, extending effective duration beyond existing therapies.

Anti-TIGIT antibodies bind human TIGIT to block CD155 and CD112 interactions, resolving T cell suppression caused by tumor immune evasion.

A micelle construct targets cancer cells via GLUT1 antibodies to deliver combination chemotherapy agents.

Blocking inhibitory KIRs with an anti-KIR antibody overcomes pediatric BCP-ALL resistance to natural killer cell lysis, improving treatment effectiveness.

Affinity matured anti-TNFRSF25 antibodies stimulate CD8+ T cell proliferation and induce tumor cell apoptosis, resolving cross-species binding limitations.

A bispecific antibody construct bridges tumor cells and T cells to enhance cytotoxic activity.

Hexamerization mutations in the antibody constant region boost CD40 agonist activity while reducing unwanted effector functions.