1. GPCR/G Protein Immunology/Inflammation
  2. CCR
  3. CAP-100

CAP-100 is a monoclonal antibody that targets CCR7. CAP-100 neutralizes the ligand-binding site and signaling of CCR7. CAP-100 strongly inhibits CCR7-induced migration, extravasation, homing, and survival in chronic lymphocytic leukemia (CLL) samples. CAP-100 triggers potent tumor cell killing, mediated by host immune mechanism. CAP-100 shows a favorable toxicity profile on relevant hematopoietic subsets. CAP-100 is involved in research on anti-tumor and disease such as CLL.

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CAP-100 Chemical Structure

CAP-100 Chemical Structure

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Description

CAP-100 is a monoclonal antibody that targets CCR7. CAP-100 neutralizes the ligand-binding site and signaling of CCR7. CAP-100 strongly inhibits CCR7-induced migration, extravasation, homing, and survival in chronic lymphocytic leukemia (CLL) samples. CAP-100 triggers potent tumor cell killing, mediated by host immune mechanism. CAP-100 shows a favorable toxicity profile on relevant hematopoietic subsets. CAP-100 is involved in research on anti-tumor and disease such as CLL[1].

In Vitro

CAP-100 (0.1-10 ng/μL) demonstrates the most potent binding to CCR7 immunogen SYM1899 (100 ng) with a EC50 of 1.78 ng/mL[1].
CAP-100 (0.01-100 μg/mL) shows dose-dependent inhibition of ligand-induced activation, reaching maximal inhibitions close to 100% in CCR7+ CHO-K1 cells stimulated with CCL19[1].
CAP-100 (0.1-100 μg/mL) binds to CCR7+ non-tumor PB or BM cells from healthy donors at high experimental concentrations[1].
CAP-100 (1-100 μg/mL) impairs the increase of D-actin upon CCL19/CCL21 stimulation in CLL cells[1].
CAP-100 (0.1-100 μg/mL, 4 h) demonstrates a strong dose-related inhibitory activity against CCR7-driven T-PLL cells migration towards 1 μg/mL of CCL19 or CCL21[1].
CAP-100 (10 μg/mL) impairs CCR7-induced migration of CCL cells in trans-endothelial migration (TEM) assays[1].
CAP-100 (10-100 μg/mL, 24 h) does not mediate direct specific-induced cell death but impairs the viability of CCR7-mediated cells which is the protective function in CLL[1].
CAP-100 (10 μg/mL) activated human NK-92-CD16+ cells to induce a strong ADCC on target CLL cells[1].

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

In Vivo

CAP-100 (10 μg/mL, i.v., one single dose) reduces in vivo homing of CCR7-expressing cells to lymph node of NSG mice[1].
CAP-100 (25-200 μg/mouse, i.v., one single dose) shows prolonged median overall survival regardless of dose and reduces tumor burden as well as reducing lymph node infiltration in Granta-519-luc+-bearing mice[1].
CAP-100 (10-200 μg/mouse, i.v., one single dose) significantly extends the lifespan of JVM-3-bearing SCID mice compared to Trastuzumab (HY-P9907) (200 μg)[1].

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

SMILES

[CAP-100]

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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  • 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.

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CAP-100
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HY-P991224
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