2. GPCR/G Protein Immunology/Inflammation
  3. CXCR
  4. PF-06747143

PF-06747143 is recombinant anti-human antibody targeting CXCR4. PF-06747143 blocks CXCL12-induced calcium flux, F-actin polymerization, chemotaxis, cell migration, and leukemic cell bone marrow homing. PF-06747143 reduces tumor burden and improves survival in mouse models of hematologic malignancies. PF-06747143 can be used for the research of chronic lymphocytic leukemia, acute myeloid leukemia, and hematologic malignancies.

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PF-06747143

PF-06747143 Chemical Structure

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Description

PF-06747143 is recombinant anti-human antibody targeting CXCR4. PF-06747143 blocks CXCL12-induced calcium flux, F-actin polymerization, chemotaxis, cell migration, and leukemic cell bone marrow homing. PF-06747143 reduces tumor burden and improves survival in mouse models of hematologic malignancies. PF-06747143 can be used for the research of chronic lymphocytic leukemia, acute myeloid leukemia, and hematologic malignancies[1][2][3][4].

Isotype

Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity

Human
IC50 & Target[1]

CXCR4

 

In Vitro

PF-06747143 (20 μg/mL) binds specifically to human CXCR4-expressing CHO-hCXCR4 cells, with no binding to CXCR4-negative CHO-parental cells[1].
PF-06747143 (110 min) potently inhibits CXCL12-induced calcium flux in Jurkat cells with an IC50 of 1.41 nM, and this inhibitory activity does not require antibody bivalency or the Fc region[1].
PF-06747143 (10-1000 nM; 48 h) induces bivalency-dependent cell death in patient-derived primary CLL-B cells, with activity independent of stromal cell support, CLL prognostic risk factors, or TP53 status, and minimal effect on normal B and T lymphocytes[1].
PF-06747143 (100 nM; 48 h) induces caspase-independent cell death in patient-derived primary CLL-B cells[1].
PF-06747143 (100 nM) induces bivalency-dependent ROS production and subsequent cell death in patient-derived primary CLL-B cells, with ROS levels comparable to the programmed cell death-inducing antibody obinutuzumab[1].
PF-06747143 (10-1000 nM) potently inhibits CXCL12-induced F-actin polymerization in primary CLL-B cells, with 100 and 1000 nM reducing polymerization below baseline levels[1].
PF-06747143 (10 nM-1 μM; 1 h pre-incubation) dose-dependently inhibits CXCL12-induced migration of primary CLL-B cells[1].
PF-06747143 (0.2-2000 nM; 4 h) induces dose-dependent complement-dependent cytotoxicity in primary CLL-B cells, with significantly greater activity in the presence of active complement[1].
PF-06747143 induces potent antibody-dependent cell-mediated cytotoxicity in primary CLL-B cells and JVM-13 CLL tumor cells, with activity dependent on the IgG1 Fc region[1].
PF-06747143 significantly inhibits CXCL12-induced chemotaxis in primary AML cells[2].
PF-06747143 (65 nM; 4-5 h) potently inhibits CXCL12-driven migration of HL-60, U937, and primary AML cells[3].
PF-06747143 (0-100 nM; 4 h) induces dose-dependent ADCC-mediated cytotoxicity in primary AML BM cells and MV4-11 cells via Fc-effector function, with activity dependent on CXCR4 expression[3].
PF-06747143 functionally antagonizes CXCL12-induced CXCR4 signaling in CHO-K1-CXCR4 cells with an EC50 of 7.75 nM[4].
PF-06747143 (24 h) potently inhibits CXCL12-induced migration of Ramos human NHL cells with an IC50 of 0.24 nM, and also inhibits migration of MV4-11 AML cells[4].
PF-06747143 (4 h) induces potent ADCC against Ramos human NHL cells with an IC50 of 115 pM[4].
PF-06747143 (100 nM; 4 h) induces ADCC-mediated cell death in MV4-11 human AML cells and OPM-2 human MM cells[4].
PF-06747143 (33 nM; 4 h) induces CDC-mediated cell lysis in Daudi human NHL cells[4].

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

PF-06747143 Related Antibodies

Cell Migration Assay [1]

Cell Line: primary CLL-B cells
Concentration: 10; 100; 1000 nM
Incubation Time: 1 h pre-incubation
Result: Significantly inhibited cell migration in a range from 40 to 80%, relative to CXCL12 induction only.
Inhibited cell migration in a dose dependent manner.
In Vivo

PF-06747143 (10 mg/kg; s.c.; once weekly; 6 doses) reduces chronic lymphocytic leukemia tumor burden and extends median survival in a disseminated murine xenograft model[1].
PF-06747143 (10 mg/kg; s.c.; weekly for 7 weeks; or single dose) inhibits tumor growth and extends median survival in the P17CXCR4-low AML mouse PDX model[3].
PF-06747143 (10 mg/kg; s.c.; weekly; 5 weeks) inhibits leukemia growth and extends median survival in the P15CXCR4-high AML mouse PDX model[3].
PF-06747143 (0.1-30 mg/kg; s.c.; weekly; 2-4 doses) induces dose-dependent tumor growth inhibition in a subcutaneous NHL xenograft model[4].

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

Animal Model: SCID beige (female, disseminated chronic lymphocytic leukemia model via tail vein injection of luciferase-expressing JVM-13 CLL cells)[1]
Dosage: 10 mg/kg
Administration: s.c.; once weekly; 6 doses
Result: Reduced tumor burden compared to IgG1 control.
Extended median survival to 68.5 days.
Animal Model: NSG mice (immunodeficient)[3]
Dosage: 10 mg/kg mobilization study)
Administration: s.c.; weekly for 7 weeks; or single dose
Result: Significantly reduced the percentage and absolute number of hCD45+ leukemic cells in peripheral blood after 2 weeks of treatment, with sustained reductions in bone marrow, spleen, and peripheral blood at study end (7 weeks).
Extended median survival to 167 days, compared to 113 days for control mice.
Reduced density of AML cells in bone marrow, spleen, and liver relative to controls.
Resulted in significantly lower peripheral blood leukemic cell percentages at 14 weeks post-secondary transplantation, and extended secondary mice median survival to 165.5 days, compared to 138 days for mice receiving control-treated cells.
Induced rapid mobilization: absolute leukemic cell numbers increased in peripheral blood and decreased in bone marrow 4 hours post-injection.
Animal Model: NSG mice (immunodeficient)[3]
Dosage: 10 mg/kg
Administration: s.c.; weekly; 5 weeks
Result: Prevented increases in peripheral blood leukemic cell percentages and absolute numbers, with sustained reductions in bone marrow, spleen, and peripheral blood at study end.
Showed leukemic burden significantly lower than both control in all tissues.
Extended median survival to 156 days.
Reduced density of AML cells in bone marrow, spleen, and liver relative to control.
Resulted in significantly lower peripheral blood leukemic cell percentages at 8 weeks post-secondary transplantation compared to control.
Animal Model: SCID beige (female)[4]
Dosage: 0.1; 1; 10; 30 mg/kg
Administration: s.c.; weekly; 2-4 doses
Result: Induced tumor regressions in 70% of animals at 10 mg/kg, with tumor volumes below initial sizes at the end of the study.
Showed similar sustained tumor growth inhibition relative to initial tumor volume at 10 mg/kg and 30 mg/kg through day 38, even after treatment suspension on day 21.
Gene ID

7852  [NCBI]

Accession
Target

CXCR4/CD184
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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PF-06747143 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:

PF-06747143PF06747143PF 06747143CXCRCXC chemokine receptorsC-X-C motif chemokine receptorsCLL-B cellshematologic malignanciesacute myeloid leukemianon-Hodgkin lymphomamultiple myelomaCXCR4Jurkat cellschronic lymphocytic leukemiaAML patient cellsCXCL12Inhibitorinhibitorinhibit

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