Imvotamab
Imvotamab (IGM-2323) is a CD20 and CD3 bispecific IGM antibody with dual action mechanism. Imvotamab is used to induce physiological T cell activation to prevent over-stimulation and subsequent down-regulation of immune function. Imvotamab can be used for the study of B-cell malignant tumors, multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2573121-53-4
-
Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
IC50 & Target
CD3E
In Vitro
Imvotamab (1-10000 pM) has Killing effect on Rituximab (HY-P9913)-resistant ramos cells[5].
Imvotamab (0.1-1000 pM) has Killing effect on standard ramos cells[5].
Imvotamab (1-1000 pM) significantly reduces the content of IL-6, IL-2, IFNγ and TNFα in cytokine release syndrome[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Imvotamab (25 mg/kg) promotes the depletion of B cells in spleen and lymphoid tissue without significant adverse effects in non-human primate[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Format
-
IgM-kappa-[scFv-heavy-kappa]-Jchain-ALB
Chemical Information
-
CAS. Nr. 2573121-53-4
-
SMILES
[Imvotamab]
-
Synonyms
IGM-2323
-
Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
-
Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)