Antibody Ingredients TRIZ Cases

Protease-cleavable masking activates T cell engager polypeptides at disease sites, reducing off-target toxicity and systemic adverse events.

Baseline NK cell count and CD16 expression help identify patients more likely to benefit from MOR00208 anti-CD19 therapy.

A CD40 binder targeting an N-terminal epitope avoids steric hindrance in bispecific conjugates, enabling antigen delivery and stronger T-cell activation.

Targeted IgA constant-region substitutions tune glycosylation to extend half-life, reduce aggregation, and boost ADCC in cancer therapy.

Engineered anti-KLK5 antibodies inhibit protease activity without competing with LEKTI, helping restore skin barrier function and reduce inflammation.

Fully human anti-BCMA antibodies use optimized CDR binding to block APRIL and inhibit BCMA-expressing myeloma cell survival.

By linking HER2 tumor binding with CD3 T-cell engagement, this case targets low-HER2 cancers resistant to PD1 and PDL1 blockade.

Targeting the IGSF1 C-terminus helps treat high-IGSF1 cancers by boosting immune cell infiltration and inhibiting tumor growth.

CD73-targeting antibodies are combined with checkpoint inhibitors to block adenosine-driven immunosuppression and strengthen anti-tumor immunity.

Engineered ABPs bind HLA-A*02:01 peptide targets to improve tumor-cell specificity and reduce off-target effects in cancer treatment.

PD-L1 tissue testing guides anti-PD-1 treatment selection, improving response prediction and avoiding ineffective cancer immunotherapy.

Engineered anti-LAG3 variable regions strengthen antigen and cell binding to boost T cell activation and cytokine release.

By combining BCMA, TCR, and CD2 or TAA binding, these molecules boost T-cell lysis and proliferation against cancerous B cells.

TNFR2-binding antagonistic polypeptides curb T-reg and MDSC suppression, expand cytotoxic T cells, and strengthen cancer immunotherapy.

Fully human anti-CLPTM1L antibodies block tumor cell apoptosis protection, improve chemotherapy response, and reduce metastasis.

High-affinity anti-Sp17 antibodies use optimized CDRs to improve specific binding to Sp17-expressing cancer cells for therapy and diagnosis.

By competitively blocking CCR5, leronlimab reduces metastatic burden and angiogenesis while limiting side effects and dosing demands.

Dual checkpoint blockade targets PD-1 and LILRB1/2 to restore CD8+ T-cell activity and overcome resistance to PD-1 monotherapy.

ICOS agonist antibodies boost T cell proliferation and cytokine release while countering exhaustion and Treg suppression in cancer immunotherapy.

High-affinity anti-CCR8 antibodies improve tumor-cell targeting and ADCC/ADCP activity while limiting off-target binding and systemic side effects.

Blocking PVRIG-CD112 with a high-affinity anti-PVRIG antibody boosts PBMC and NK cell killing while inhibiting tumor growth.

A masking moiety and cleavable linker keep anti-PDL1 antibodies inactive until protease activation, reducing off-target toxicity.

Fc-engineered anti-CD40L antibodies block CD40L-CD40 binding while avoiding platelet activation, complement binding, and thromboembolic risk.

A humanized anti-CD73 binding protein improves enzyme blocking, supports T cell proliferation, and maintains stable serum levels for tumor therapy.

Blocking PVRIG and TIGIT with single-domain and bispecific antibodies boosts T cell and NK cell activity to inhibit tumor growth.

CD3 affinity tuning preserves tumor cell killing while reducing cytokine storm, immunogenicity, and dose-limiting toxicity.

Engineered PD-L1 antibodies improve binding and internalization, enabling targeted payload delivery while modulating PD-L1/PD-1 immune signaling.

A low-pH antibody formulation uses buffers, saccharides, and surfactants to reduce aggregation and support stable high-concentration dosing.

Specific CDR sequence design improves human OX40 binding, enabling anti-OX40 antibodies to activate or inhibit T-cell responses.

Blocking HJV with subcutaneous antibodies lowers hepcidin and restores serum iron to address functional iron deficiency in myelofibrosis.

Blocking MMP-2 and MMP-13 cleavage of CD28 lowers soluble CD28, preserves membrane CD28, and supports PD-1 and PD-L1 immunotherapy.

Combining an anti-PD-L1 antibody with a c-Met kinase inhibitor helps overcome primary resistance in low PD-L1 tumors.

Specific CD19-binding antibody variants improve tumor targeting and therapeutic efficacy while limiting toxicity from non-specific binding.

A buffered liquid anti-PCSK9 antibody formulation uses surfactant, sucrose, and optional arginine to limit aggregation, preserve potency, and keep viscosity suitable for administration.

Humanized anti-Nectin-2 antibodies use Fc mutations and cytotoxic conjugates to preserve tumor targeting while reducing immune response and toxicity.

ZIP12-targeting antibodies block hypoxia-driven zinc transport and cell proliferation while enabling less invasive pulmonary hypertension diagnosis.

Adding cyclodextrin to polypeptide formulations helps solubilize polysorbate degradation products, reducing particles and extending stability.

Tumor-specific covalent neoantigens let antibodies recognize intracellular oncoproteins on cell surfaces without MHC allele restriction.

A monovalent CD47-binding format blocks CD47/SIRPα interactions and kills tumor cells without the hemagglutination seen with conventional antibodies.

Bispecific BCMA-CD3 antibodies deplete plasma cells to lower anti-HLA alloantibodies and cPRA, helping highly sensitized transplant patients.

TfR-binding anti-HER2 bispecific antibodies cross the blood-brain barrier to target HER2-positive brain metastases more effectively.

FAP-targeted LTBR agonists combined with anti-CD3 engagers improve T cell infiltration in solid tumors by reshaping the microenvironment.

Fc-effector-null anti-CD137 antibodies boost T-cell and NF-kappa B activity to improve tumor response while limiting immune-related toxicity.

A symmetric CEA×CD3 antibody format reduces immunogenicity, soluble CEA interference, and CEACAM cross-reactivity while improving tumor killing.

An anti-claudin-3 antibody targets SCLC cells with high ADCC while sparing normal cells, reducing side effects and improving treatment specificity.

Antibodies bind neoantigen drug-peptide conjugates on MHC I to target intracellular oncoproteins with higher specificity and fewer off-tumor effects.

Lyophilized anti-PD-1 antibody formulations use histidine, sucrose, and polysorbate 80 to extend shelf-life while preserving bioactivity.

Native-form CCR8 immunization with DNA, mRNA, and overexpressing cells yields antibodies with stronger binding, blocking, and tumor-cell killing.

A built-in recovery unit binds released payloads in ligand-drug conjugates, lowering off-target toxicity while widening the therapeutic window.

Epitope-specific CEACAM5 antibodies target the A2-B2 domain to avoid CEACAM cross-reactivity while improving tumor cell killing.

Non-agonist 4-1BB nanobodies paired with Claudin 18.2 binding localize immune activation to tumors and reduce off-tumor toxicity.

Monovalent CD28 binding with bivalent tumor targeting enables localized T cell activation and killing while limiting systemic toxicity.

Low-dose IgE unit formulations adapt antibody dosing to IgE pharmacokinetics, reducing side effects and drug use in cancer treatment.

Engineered anti-CD73 antibody variants inhibit CD73 activity and trigger internalization to improve anti-tumor immune response.

Blocking LILRB1 with a specific antibody prevents MHC Class I-driven immune evasion and restores anti-cancer immune activity.

Radiolabeled BC8 antibodies selectively deplete CD45-positive cells while sparing hematopoietic stem cells to support treatment and graft engraftment.

Subcutaneous anti-HJV antibody dosing lowers hepcidin and improves iron availability in myelofibrosis while limiting Cmax-related off-target effects.

A TEM8-targeted antibody is engineered to combine high specificity, strong binding, and endocytosis for ADC and CAR-T use.

A protease-resistant linker joins PD-L1 IgG and B7H3 nanobodies to improve bispecific antibody stability and anti-tumor activity.