Antibody Ingredients TRIZ Cases

Bispecific PD-L1×CD137 antibodies block PD-1/PD-L1 while activating CD137 to boost T cell responses without Fc-mediated cytotoxicity.

Single-domain VHH antibodies block PD-L1-PD-1 signaling with high selectivity, stability, and cytokine induction for immunotherapy use.

Prevalidated PIK3CA H1047R mutant peptides improve tumor immunogenicity and enable broader T-cell targeting without patient-specific screening.

Broad-specificity anti-SIRPα antibodies bind both SIRPα variants to block CD47 signaling and boost macrophage phagocytosis of tumor cells.

Targeting a specific TGF-βRII extracellular epitope blocks ligand binding and signaling while avoiding cytokine release syndrome.

Five novel anti-CD73 antibodies target distinct epitopes to improve enzyme inhibition, binding affinity, and tumor suppression.

Selective CD45+ host cell depletion clears the way for hematopoietic stem cell engraftment while limiting harmful immune effector activity.

Fc-engineered BCMA×CD3 bispecific antibodies improve tumor targeting while reducing cytokine release, toxicity, and short half-life.

Inert complementing domains stabilize split effector binders so T cell activity assembles on target cells, reducing toxicity and aggregation.

A dual-binding antibody uses BBB endothelial targeting plus brain-specific binding to raise brain exposure and retention despite rapid clearance.

Dual-target antibody drug conjugates bind cMET and EGFR to address acquired resistance and improve efficacy in EGFR/cMET-associated diseases.

An hK2-targeted CD3 bispecific redirects T cells to prostate tumors while lowering CRS and off-tumor toxicity for outpatient dosing.

Targeting G-CSF signaling helps reduce vaso-occlusion and vascular stasis in sickle cell disease where current therapies face efficacy and side-effect limits.

Controlled pH, pCO2, temperature, and defined media enable commercial rat hybridoma antibody production with higher yield and lower fucosylation.

By binding GPRC5D on myeloma cells and CD3 on T cells, this bispecific antibody improves anti-tumor efficacy with a single therapeutic format.

Multispecific antibodies bridge Vδ1+ gamma delta T cells to tumour or immunomodulatory targets, boosting cytotoxicity with lower off-target toxicity.

Selective CEACAM5 A2-B2 binding avoids CEACAM1/6/8 cross-reactivity while stable immunoconjugates improve tumor killing and systemic stability.

Radiolabeled humanized hK2 antibodies target prostate micrometastases while improving tumor-to-bone marrow dose ratios and limiting healthy tissue damage.

Early anti-IgE dosing in pregnancy or infancy suppresses allergen-specific IgE and helps prevent later allergic disorders.

Specific CXCR2 binding blocks CXCL8 signaling to curb tumor growth, metastasis, and support diagnosis in CXCR2-overexpressing cancers.

Combining a Wnt pathway inhibitor with anti-PD-1 helps eliminate resistant tumor cells by boosting lymphocyte infiltration and reducing side effects.

Anti-CD39 antibodies induce target cytosis to remove CD39 on immune cells, restore T-cell function, and suppress tumor growth.

Blocking Galectin-9 and Tim-3 signaling restores T-cell effector function in ETP T-ALL and may improve response to chemotherapy.

Elevated serum succinate reveals NSCLC progression, while anti-succinate antibodies or SUCNR1 inhibition suppress TAM polarization and metastasis.

Engineered CHO cells deliver IgG1 and IgG3 antibodies with 99% fucosylation and low N-glycan impurities to improve ADCC and CDC.

Targeted Fc-domain substitutions boost acidic FcRn binding to extend antibody half-life while preserving ADCC activity.

A buffered CEACAM5 ADC formulation using sorbitol, polysorbate 80, and optional EDTA improves huMAb2-3-SPDB-DM4 stability and shelf life.

Engineered FcRn antigen-binding molecules lower serum IgG while preserving albumin levels and extending half-life to reduce dosing frequency.

Temperature- and pH-based de-glycation kinetics predict protein glycation over time and guide glucose formulation to preserve therapeutic potency.

Bispecific antibodies bridge TRDV2-positive γδ T cells and tumor antigens to drive specific cancer cell lysis with lower side effects.

Encapsulating antibodies in low-PDI liposomes enables sustained subcutaneous delivery with higher bioavailability, longer half-life, and lower immunogenicity.

Using chicken immunization to target divergent hCD20 epitopes, this case shows stronger ADCC and CDC for improved B lymphoma cell depletion.

Dual TAA-TNFR2 binding overcomes monoclonal cross-linking limits to activate CD8+ T cells or suppress Treg proliferation.

Non-fucosylated PD-1 agonist antibodies enhance Fc receptor binding to deplete immune cells and suppress T cell activation in inflammatory disease.

Combining a RAS(ON) inhibitor with pathway, kinase, or immunotherapy agents helps overcome resistance and extend response durability in RAS-driven cancers.

Humanized CTLA4-binding protein combinations boost T cell activation and CTLA4 blockade while aiming to lower toxicity seen with ipilimumab.

Subcutaneous mosunetuzumab plus polatuzumab vedotin improves CD20-positive disorder treatment while reducing cytokine and infusion toxicities.

A modular bispecific format combines knobs-in-holes assembly and single-chain Fab expression to target IL-6Rα and IL-8R for metastasis inhibition.

Optimized anti-CTLA4 CDR sequences raise binding affinity and CTLA4 blocking activity to strengthen T cell responses and tumor inhibition.

Blocking TIGIT with an antibody restores effector T cell activity, reduces immune suppression, and strengthens anti-tumor responses.

Agonistic anti-MuSK antibodies directly activate MuSK to restore AChR clustering and neuromuscular junction function despite pathway defects.

Alanine-scanned CDR sequence changes improve CD3 binding affinity and specificity in recombinant antibodies for therapeutic targeting.

Subcutaneous anti-HJV antibodies suppress hepcidin-25 in myelofibrosis while limiting Cmax, off-target effects, and sharp serum iron spikes.

Combining PD-L/PD-1 antagonists with immune-cell activators sustains tumor killing by overcoming long-term antibody tolerance and blockade limits.

A cleavable peptide masks CD3 binding during circulation, then tumor proteases activate the antibody to limit off-target tissue binding.

An anti-Trop2 antibody linked to NK cells targets high-Trop2 tumors to improve tumor killing while reducing toxic side effects.

Specific monoclonal MUC1* antibodies replace variable polyclonal mixes to reproducibly stimulate or block receptor-driven cell growth.

Dual EGFR and MUC1-C binding improves tumor selectivity, avoids shed MUC1-N off-target binding, and reduces normal-tissue side effects.

By replacing key antibody CDR regions, this case enables strong canine CTLA-4 binding and blocks CD80/CD86 signaling to support cancer therapy.

Targeting CSF-1R with axatilimab treats chronic graft versus host disease while reducing toxicity and broad immunosuppression.