2. JAK/STAT Signaling Protein Tyrosine Kinase/RTK Immunology/Inflammation PI3K/Akt/mTOR MAPK/ERK Pathway Apoptosis
  3. EGFR CD3 PI3K Akt p38 MAPK Caspase Apoptosis IFNAR TNF Receptor Interleukin Related
  4. M802

M802 is an anti-HER2/CD3 bispecific antibody, with a Kd of 0.578 nM for human HER2 and a Kd of 71.2 nM for human CD3. M802 inhibits the PI3K/AKT and MAPK signaling pathways, suppresses tumor cell proliferation, activates caspase-3, and promotes tumor cell apoptosis (apoptosis). M802 recruits and activates CD3-positive immune cells, mediates cytotoxicity against HER2-positive tumor cells, and induces immune cells to secrete IFN-γ, TNF-α, IL-2 and IL-6. M802 exhibits anti-tumor efficacy in mice with gastric cancer xenografts. M802 can be used in research related to HER2-positive breast cancer, HER2-positive gastric cancer and other cancers. The recommended isotype control is human IgG1 kappa (HY-P99001).

For research use only. We do not sell to patients.

M802

M802 Chemical Structure

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M802 Related Antibodies

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Description

M802 is an anti-HER2/CD3 bispecific antibody, with a Kd of 0.578 nM for human HER2 and a Kd of 71.2 nM for human CD3. M802 inhibits the PI3K/AKT and MAPK signaling pathways, suppresses tumor cell proliferation, activates caspase-3, and promotes tumor cell apoptosis (apoptosis). M802 recruits and activates CD3-positive immune cells, mediates cytotoxicity against HER2-positive tumor cells, and induces immune cells to secrete IFN-γ, TNF-α, IL-2 and IL-6. M802 exhibits anti-tumor efficacy in mice with gastric cancer xenografts. M802 can be used in research related to HER2-positive breast cancer, HER2-positive gastric cancer and other cancers. The recommended isotype control is human IgG1 kappa (HY-P99001)[1].

Isotype

Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity

Human
IC50 & Target[1]

Human HER2

0.578 nM (Kd)

IL-6

 

Caspase 3

 

IL-2

 

TNF-α

 

In Vitro

M802 (0-50 nM) specifically binds to the purified extracellular domains of human HER2 and CD3, with high affinity for HER2 (Kd = 0.578 nM) and lower affinity for CD3 (Kd = 71.2 nM), and possesses dual binding capacity to simultaneously bind both antigens[1].
M802 (0.001-1000 nM; 1 h for single cell binding; 0-10 μg/mL; 30 min for co-binding) specifically binds to HER2 on SK-BR-3 cells (Kd = 11.71 nM) and CD3 on Jurkat cells (Kd = 186.8 nM), and mediates dose-dependent formation of cell aggregates between HER2-positive tumor cells and CD3-positive T cells[1].
M802 (0-108 pg/mL; 48 h) mediates potent, dose-dependent PBMC cytotoxicity against HER2-positive SK-BR-3, BT-474, NCI-N87 and JIMT-1 tumor cells, while exhibiting extremely low activity against HER2-negative MDA-MB-231 cells and non-cancerous HEK-293 cells[1].
M802 (0.01-10 μg/mL; 0-6 days) inhibits the proliferation and promotes the apoptosis of HER2-positive SK-BR-3 and BT-474 breast cancer cells in a dose-dependent manner, but has no effect on the proliferation of JIMT-1 cells[1].
M802 (0.1-10 μg/mL; 24-48 h) dose-dependently modulates the PI3K/AKT and MAPK signaling pathways, inhibits kinase phosphorylation, regulates cyclins, and activates the apoptotic cleavage of caspase-3 in HER2-positive SK-BR-3 and BT-474 breast cancer cells[1].
M802 (0.0001-10000 ng/mL; 48 h) activates T cells in a dose-dependent manner and induces the secretion of IFN-γ, TNF-α, IL-2 and IL-6 when co-cultured with HER2-positive SK-BR-3 tumor cells and human peripheral blood mononuclear cells (PBMCs)[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

M802 Related Antibodies

Cell Cytotoxicity Assay[1]

Cell Line: human breast cancer SK-BR-3, BT-474, JIMT-1, MDA-MB-231 cells, human gastric cancer NCI-N87 cells, human embryonic kidney HEK-293 cells, peripheral blood mononuclear cells (PBMCs)
Concentration: 0-105 pg/mL (SK-BR-3, NCI-N87, BT-474, JIMT-1); 10-2-108 pg/mL (MDA-MB-231); 100-105 pg/mL (HEK-293)
Incubation Time: 48 h
Result: Induced potent, dose-dependent cytotoxicity against HER2-positive SK-BR-3 (EC50 = 782.7 pg/mL, maximum lysis = 74.71%).
Induced potent, dose-dependent cytotoxicity against HER2-positive BT-474 (EC50 = 2808 pg/mL, maximum lysis = 93.90%).
Induced potent, dose-dependent cytotoxicity against HER2-positive NCI-N87 (EC50 = 833.9 pg/mL, maximum lysis = 78.40%).
Induced potent, dose-dependent cytotoxicity against Herceptin-resistant JIMT-1 (EC50 = 39365 pg/mL, maximum lysis = 94.89%).
Showed minimal cytotoxicity against HER2-negative MDA-MB-231 (maximum lysis = 50.58%).
Showed minimal cytotoxicity against non-cancerous HEK-293 (maximum lysis = 12.78%).

Cell Proliferation Assay[1]

Cell Line: human breast cancer SK-BR-3, BT-474, and JIMT-1 cells
Concentration: 0.01, 0.1, 1, 10 μg/mL
Incubation Time: 0-6 days
Result: Exhibited dose-dependent inhibition of proliferation in SK-BR-3 and BT-474 cells, with effects becoming apparent after day 4, though this inhibition was weaker than that of Herceptin.
Had no inhibitory effect on Herceptin-resistant JIMT-1 cell proliferation.

Apoptosis Analysis[1]

Cell Line: human breast cancer SK-BR-3, BT-474, and JIMT-1 cells
Concentration: 0.1, 1, 10 μg/mL
Incubation Time: 48 h
Result: Significantly increased the apoptotic ratio of SK-BR-3 and BT-474 cells in a dose-dependent manner, with the highest effect at 10 μg/mL.
Showed no statistically significant difference in apoptosis induction in JIMT-1 cells compared to Herceptin, and neither induced meaningful apoptosis in this resistant cell line.

Western Blot Analysis[1]

Cell Line: human breast cancer SK-BR-3, BT-474, and JIMT-1 cells
Concentration: 0.1, 1, 10 μg/mL
Incubation Time: 24 h (Akt/p-Akt, Erk/p-Erk); 48 h (cyclin D1, p21, p27, caspase-3, cleaved-caspase-3)
Result: Caused dose-dependent inhibition of Akt and Erk phosphorylation, downregulation of cyclin D1, upregulation of p21 and p27, and increased levels of cleaved-caspase-3 in SK-BR-3 and BT-474 cells.
Had no effect on p-Akt or p-Erk levels in JIMT-1 cells.
Parmacokinetics
Species Dose Route CL Cmax T1/2β
Mice[1] 8 mg/kg i.v. 2.432×10-6 L/h/kg 69747.167 ng/mL 63.665 h
In Vivo

M802 (1-2 mg/kg; i.v.; bolus injection on day 0, day 2, day 4) exhibits potent dose-dependent antitumor efficacy in NOD/SCID mice with NCI-N87 gastric cancer xenografts[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: NOD/SCID (female, 7 to 8 weeks old)[1]
Dosage: 1 mg/kg; 2 mg/kg
Administration: i.v.; bolus injection on day 0, day 2, day 4
Result: Achieved complete inhibition of tumor growth throughout the 53-day observation period (2 mg/kg).
Showed significant tumor growth inhibition, with small nodules observed only during the later period of the study, and an inhibitory effect similar to that of 4 mg/kg Herceptin (1 mg/kg).
Gene ID

2064  [NCBI] & 916  [NCBI]

Accession
Target

ERBB2/HER2/CD340 & CD3
Application

ELISA, FACS, Functional assay
Conjugated

Unconjugated
Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.
Formulation

Please refer to the lot-specific COA for specific buffer information.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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M802 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

M802M 802M-802EGFRCD3PI3KAktp38 MAPKCaspaseApoptosisIFNARTNF ReceptorInterleukin RelatedEpidermal growth factor receptorErbB-1HER1Cluster of differentiation 3Phosphoinositide 3-kinasePKBProtein kinase BInterferon-α/β receptorInterferon-alpha/beta receptor Tumor Necrosis Factor ReceptorTNFRILHerceptin-resistant breast cancerNOD/SCID miceMAPK signaling pathwaysPI3K/AKT signaling pathwaysSK-BR-3 cellsHER2-positive gastric cancerHER2Jurkat cellsHER2-positive breast cancerInhibitorinhibitorinhibit

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