Antibody Ingredients TRIZ Cases

A Claudin 6-targeted antibody-drug conjugate delivers maytansine to liver cancer cells, improving specificity while limiting harm to normal tissues.

Triggered linker conjugates form a 5-6-membered ring to release active agents selectively in tumor cells while limiting harm to healthy cells.

Optimized anti-CD3 CDR sequences improve expression, stability, solubility, and half-life while supporting effective T cell activation.

A Lewis Y-targeted 225Ac radio-conjugate replaces toxic antibody warheads to improve tumor killing while limiting normal tissue exposure.

Antibodies engineered to bind Fuc-GM1 glycolipid but not free sugar improve SCLC targeting while reducing GM1 cross-reactivity and adverse reactions.

Targeting the ILT3 pathway with Q3W anti-ILT3 antibodies may reduce CMML and AML progression while avoiding transplant-related complications.

Multispecific molecules bridge IgG and ASGR1 to speed lysosomal IgG clearance, reduce frequent high dosing, and limit off-target effects.

Bispecific antibodies bridge EGFR and ITGB6 to degrade cell surface EGFR, extending event-driven pharmacology beyond intracellular targets.

Combining anti-BCMA CAR-T cells with a GPRC5D×CD3 bispecific antibody helps extend response and sustain MRD-negativity in multiple myeloma.

Site-specific cysteine insertion enables homogeneous antibody-drug conjugates with controlled DAR, improving stability, specificity, and pharmacokinetics.

An anti-CD20 ADC plus CHP regimen improves NHL efficacy while cutting drug count, infusion time, safety risks, and cost.

Blocking ILT2 and ILT4 with antibodies restores myeloid FcR activation and boosts NK, CTL, and macrophage attack on cancer cells.

Humanized anti-5T4 antibodies use CDR-based high-affinity binding and rapid internalization to target 5T4-overexpressing cancers.

Novel camptothecin derivatives and antibody-drug conjugates improve tumor inhibition while reducing hematotoxicity and gastrointestinal side effects.

Optimized anti-BCAM CDR sequences improve BCAM binding and cancer-cell internalization, enabling more targeted antibody-drug conjugates.

Reduced CD3 binding and asymmetric bispecific valency preserve tumor cell killing while lowering cytokine release syndrome risk.

Site-specific linker chemistry and tetrapeptide cleavage improve ADC targeting and payload release in selected cancer cells.

A low-affinity CD47 and high-affinity CD20 bispecific antibody targets tumor cells, limits tissue sink effects, and reduces hematologic toxicity.

Targeting CD103+ tumor-infiltrating T cells with anti-CD103 antibodies can strengthen tumor cell interaction and improve immunotherapy response.

Targeted CelTOS epitopes, adjuvants, and pore-forming variants strengthen immune response and extend protection against parasite traversal.

CDR-optimized humanized anti-BCMA antibodies improve affinity, specificity, and internalization while lowering immunogenicity for targeted cell killing.

Dual-affinity CD19/CD38 antibodies selectively eliminate immunosuppressive B cells to improve anti-tumor response while limiting anemia and lymphopenia.

Targeted CD33 radioconjugates deplete immunosuppressive MDSCs to strengthen antitumor immune response in solid and hematologic cancers.

A c-kit-specific antibody replaces multi-target kinase inhibition to curb angiogenesis and cancer with fewer off-target side effects.

Bispecific IL10Rα/IL2Rγ binders drive selective T cell activation while reducing macrophage activation and anemia risk.

Combining glycan-depleted polyclonal antibodies with anti-PD1 or anti-PDL1 helps overcome cold-tumor resistance while limiting toxicity.

Combining PD-1 axis antagonists with taxanes boosts CD8+ T cell activity, suppresses Treg function, and improves tumor growth inhibition.

Selective CCR8 targeting removes tumor-infiltrating Tregs that blunt radiation-induced CD8+ T cell activity while avoiding pan-Treg immune risks.

High-affinity anti-Fucosyl-GM1 antibodies target SCLC tumor cells to overcome chemo-refractory relapse with lower normal-tissue toxicity.

Dual c-Kit and CD203c binding enables mast cell depletion while limiting bone marrow suppression from indiscriminate c-Kit inhibition.

These trispecific antibody constructs bind CD3, CD28, and tumor antigens to boost T cell activation against low-infiltration tumors.

Recombinant anti-CSP antibodies target Plasmodium falciparum to bypass drug resistance, cut liver parasite load, and improve survival.

Fully human 191P4D12-targeting ADCs improve cancer targeting while reducing HAMA response and extending antibody half-life.

Blocking FcRn-mediated IgG recycling lowers pathogenic autoantibodies in primary Sjögren's syndrome while improving gland function and symptoms.

Anti-CEA antibodies covalently linked to benzazepine derivatives improve access to inaccessible tumors while boosting immune response.

Engineered humanized antibodies block Notch3 ligand binding to improve specificity, reduce immunogenicity, and inhibit tumor growth and PAH.

Specific CDR-engineered anti-IgE binding proteins block FcεRIα/FcεRII binding while improving stability and dosing duration.

Elevated extracellular NAD drives ICI resistance in HCC; blocking NAMPT or P2X7R helps restore T cell activity and improve response.

Engineered anti-CD96 hypervariable regions improve binding specificity and block CD96-CD155 immune inhibition to support antitumor response.

Blocking VISTA-VSIG3 signaling with IgG4 anti-VISTA antibodies restores T cell activation and helps address resistance across multiple cancers.

A disulfide-stabilized TfR1 binder targets the protease-like domain to avoid aggregation, preserve TfR1 function, and improve BBB transport.

Affinity-matured anti-Galectin-9 antibodies improve binding, suppress Treg expansion, and restore effector T cell activity in cancer.

Targeting the N-terminal region of BSSL shrinks tumors and inhibits metastasis while preserving lipolytic activity.

By blocking ADAM17 cleavage of CD16a, these antibodies preserve NK cell and macrophage activity to strengthen ADCC and cancer cell clearance.