Antibody Ingredients TRIZ Cases

Blocking IL-36α-, IL-36β-, and IL-36γ-mediated signaling, these antibodies target IL-36R selectively for inflammatory disease therapy.

TIM3 monoclonal antibodies block PtdSer binding linked to T cell exhaustion, supporting stronger cytokine production and antitumor immunity.

Chimeric and humanized BC8 antibodies retain CD45-positive cell targeting while reducing infusion toxicities and HAMA responses in immunotherapy.

Variable responses to PD-1/PD-L1 therapy motivate anti-PVRIG antibodies that block PVRIG-PVRL2 signaling and restore immune activation.

Multivalent VHH agents combine CD36, PD-1, and CD47 targeting to improve tumor-cell avidity and address short therapeutic half-life.

Specific CDR sequences inhibit Gas6–MerTK binding while minimizing TULP1 interaction, supporting tumor suppression with reduced ocular toxicity.

Targeted SEZ6 delivery of a Top1 inhibitor addresses limited treatment effectiveness in refractory SCLC, CNS, and neuroendocrine tumors.

Cleavable masking motifs block CD3 binding in healthy tissues and unmask antibodies in tumors, reducing cytokine release risk.

CD3 bispecific antibodies can show poor clinical efficacy in solid tumors; pairing CD3 and 4-1BB targeting reduces T-cell exhaustion and supports later tumor killing.

Combining CD27 binding with CD40/CD137 engagement strengthens costimulatory signaling and antitumor immune response in cancer therapy.

Combines anti-CAA antibodies with intrinsic or extrinsic apoptosis agents to increase cancer cell killing and promote tumor regression.

Specific antibodies bind extracellular ZIP12 to support blood-based pulmonary hypertension diagnosis and targeted therapy research.

By suppressing IgE and receptor expression, ligelizumab supports sustained desensitization across food allergens and idiopathic anaphylaxis.

Disulfide bonds linking VH and VL cysteines stabilize scFv molecules, improve expression yields, and support antigen binding.

Monoclonal antibodies target IFITM2/3 N-terminal domains to inhibit SARS-CoV-2 entry with reduced side effects.

Combining CD24 and 4-1BB binding in one protein supports ADCC, ADCP, CD8+ T-cell activation, and stronger anti-tumor responses.

Engineered heavy- and light-chain CDRs improve PD-L1 binding specificity while limiting off-target reactivity in cancer therapy.

Specific TNFR2 binding targets suppressive Treg cells, promotes CD8+ T-cell activation, and supports antitumor activity with chemotherapy.

Step-up dosing before every-three-week maintenance helps manage cytokine release syndrome while treating refractory multiple myeloma.

Mesothelin CAR cells target tumors while PD-L1 inhibition strengthens immune activation for improved tumor progression control.

A limited C-terminal amino acid addition to ISVs reduces aspecific protein interference and false signals in ADA assays.

High tumor-site adenosine activates CTLA-4 binding, while lower systemic levels help limit autoimmune reactions.

Humanized anti-CLEC-1A antibodies block ligand binding to increase tumor-cell phagocytosis by dendritic cells and macrophages.

Binding CTLA4 outside the ligand site helps limit endocytic degradation, preserve cell-surface CTLA4, and sustain ADCC.

Anti-TMEM219 antibodies block IGFBP3 binding to TMEM219, targeting colorectal cancer progression while reducing tumor density and size.

A calcium homeostasis disruptor followed by a selective DR5 agonist removes senescent cells while limiting tumor growth and metastasis.

PAR4 antibodies block thrombin activation and remain effective against Ala120 and Thr120 receptor variants, addressing PAR1 safety limits.

Anti-MIS antibodies such as B10 block MIS signaling through ALK2 and ALK3, suppressing ovarian cancer cell viability.

Bispecific antibodies bridge FcεR1α-expressing mast cells or basophils with CD3-bearing T cells to direct activation and cell lysis.

Cancer heterogeneity is addressed by using the same radiolabelled VHH fragment to confirm tumor binding before targeted isotope therapy.

Engineered CD123-binding polypeptides recruit T-cell receptors for redirected cytotoxicity while reducing cytokine release and adverse effects in AML.

Anti-DEspR antibodies selectively clear dysregulated activated neutrophils, limiting NET release, tissue injury, and organ dysfunction.

Humanized PSA-binding antibody polypeptides target tumor-associated PSA to improve micrometastasis coverage while limiting normal-organ toxicity.

Modified CDRs help antibodies bind ILT3 while limiting ILT5, ILT7, ILT8, and ILT11 cross-reactivity.

PD-L1 antibodies and CD40 agonists target dendritic cells to improve maturity, antigen presentation, and antigen-specific T-cell amplification.

Engineered Fc regions favor activating Fcγ receptors while TNFR2 binding blocks TNF-α signaling, supporting Treg depletion and anti-tumor immunity.

VISTA-mediated suppression weakens T cell activity in tumors; anti-VISTA antibodies and fragments block this signal to strengthen anti-tumor immunity.

A symmetric 1:1 format balances CEA and CD3 binding to limit immunogenicity and cytokine release while resisting soluble CEA interference.

Optimal-affinity anti-CD137 antibodies are paired sequentially with PD-1 antagonists to increase tumor immunity while limiting hepatotoxicity.

Bivalent VHH assemblies address rapid renal clearance while preserving tissue penetration for tumor and immune-cell targeting.

Direct CD200R1 binding targets tumor-infiltrating immune cells, blocking inhibitory signaling and restoring T-cell and myeloid function.

ctDNA identifies microscopic disease missed by imaging, while CSF-1/CSF-1R inhibitors target MRD before recurrence.

Dual-binding antibody domains connect ROR1-positive cancer cells with immune effectors, redirecting cytotoxicity while moderating cytokine release.

CDR sequence changes create high-affinity anti-LAG3 antibodies that block MHC class II, FGL1, and LSECtin.

See how anti-PAR2 antibodies target extracellular receptor regions to block both protease- and peptide-mediated activation.

Specific TL1A epitope binding forms smaller immune complexes, helping reduce immunogenicity while preserving therapeutic neutralization.

Engineered fully human antibodies bind PD-L1 at Kd ≤10−9 M, block PD-1 interaction, and support immune activation with reduced effector function.

Modified HVR sequences preserve LAG3 binding while increasing granzyme B and IL-2 release to strengthen T-cell effector functions.

Antibody carriers bind PROTAC VHL degrons to improve tissue-specific delivery, extend circulation, and limit non-specific degradation.

An acetate buffer at pH 4.9–5.5 helps stabilize a heterogeneous anti-HER3 antibody-drug conjugate while preserving therapeutic efficacy.