JS007
JS007 is a humanized IgG1 monoclonal antibody and also a CTLA-4 binder, with a Kd of 0.21 nM for CTLA-4. JS007 blocks the interaction between CTLA-4 and B7-1. JS007 activates T cells, promotes increased IL-2 secretion, and inhibits tumor growth in CTLA-4 knock-in mouse syngeneic tumor models. JS007 is applicable to research related to cancer and advanced solid tumors.
Para uso exclusivo en investigación. No vendemos a pacientes.
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Almacenamiento:
Please store the product under the recommended conditions in the Certificate of Analysis.
Actividad biológica
Descripciòn
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
[1]|
IL-2 |
In Vitro
JS007 binds to CHO-CTLA-4 cells with an EC50 of 0.22 μg/mL, and its binding affinity is higher than that of the control antibody Ipilimumab (HY-P9901)[1].
JS007 binds to recombinant CTLA-4 with a KD value of 0.21 nM, and its binding affinity is significantly higher than that of the control antibody Ipilimumab[1].
JS007 blocks the interaction between CTLA-4 and B7-1 in CHO-CTLA-4 cells, with an IC50 of 1.096 μg/mL[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
JS007 (0.03-0.1 mg/kg; i.p.; twice weekly) provides substantial in vivo tumor suppression efficacy in H22 syngeneic tumor-bearing human CTLA-4 knock-in BALB/c mice, with statistically significant reductions in tumor volume and weight compared to the isotype control group (p < 0.01)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6-CTLA4tm1(CTLA4)/Bcgen[1]
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Dosage:0.1 mg/kg; 1 mg/kg
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Administration:i.p.; twice weekly
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Result:Showed significantly lower tumor volume and weight compared to the isotype control group at 1 mg/kg, with values also significantly lower than the ipilimumab 1 mg/kg group (p < 0.05).
Showed significantly lower tumor volume and weight compared to the isotype control group at 0.1 mg/kg, but higher tumor volume and weight than the 1 mg/kg JS007 group.
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Animal Model:BALB/c-Ctla4em1(hCTLA4)Smoc[1]
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Dosage:0.03 mg/kg; 0.1 mg/kg
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Administration:i.p.; twice weekly
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Result:Showed substantially lower tumor volume and weight compared to the isotype control group at 0.1 mg/kg (p < 0.01).
Showed significantly lower tumor volume and weight compared to the isotype control group at 0.03 mg/kg, but higher tumor volume and weight than the 0.1 mg/kg JS007 group.
Showed a better tumor inhibition trend than ipilimumab at 0.1 mg/kg, though the difference was not statistically significant (p > 0.05).
Ensayo clínico
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Gene ID
Accession
Target
CTLA4
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Aplicación
ELISA, FACS, Functional assay
Chemical Information
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SMILES
[JS007]
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Almacenamiento
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocolo
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Gene Editing
Gene editing modify specific sites within the genome through gene deletions, insertions or conversions to study functionally unknown genes or conduct gene therapy. It is also used to change the biological traits of organisms to establish new varieties. Gene editing techniques include zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas 9) (CRISPR/Cas9).
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Patient-Derived Xenograft (PDX)
Patient-derived xenograft (PDX) models are generated by engrafting primary human tumor tissue directly into immunodeficient mice, allowing in vivo propagation of patient tumor biology without initial in vitro adaptation. These models are used to preserve key histopathological and molecular characteristics of the original tumor and enable assessment of tumor growth dynamics and therapeutic response in a living organism. The biological readout is tumor engraftment and subsequent growth in the murine host, which reflects the ability of human tumor cells to survive, vascularize, and expand in an immunocompromised microenvironment.
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Patient-Derived Orthotopic Xenograft (PDOX)
Patient-derived orthotopic xenograft (PDOX) modeling implants fresh patient tumor tissue or patient-derived tumor cells into the anatomically corresponding organ or tissue site of immunodeficient mice, usually by surgical orthotopic implantation, to preserve patient tumor histology, local microenvironmental context, invasion, metastatic behavior, and treatment-response features better than subcutaneous implantation. PDOX readouts include tumor engraftment, orthotopic tumor growth, local invasion, metastasis, recurrence after resection, histologic similarity to the donor tumor, biomarker retention, molecular concordance, survival, and response or resistance to therapy. PDOX models are used for preclinical drug testing and individualized therapy evaluation, but engraftment success varies by tumor type and specimen quality.
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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CRISPR-Cas9 mouse zygote editing
CRISPR-Cas9 mouse zygote editing introduces Cas9 nuclease and guide RNA into one-cell embryos so that Cas9 creates a guide-directed double-strand break at the target locus; repair by non-homologous end joining can generate indels, while repair with an added donor template can generate defined knock-in or point-mutation alleles. The readout is embryo, pup, or founder genotype, usually assessed by PCR, restriction-fragment analysis, Sanger sequencing, TIDE/sequence-trace analysis, or targeted sequencing; successful editing is interpreted as the presence of indels, intended HDR alleles, or both at the target locus.
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Orthotopic Cell-Line Xenograft
Orthotopic cell-line xenograft models involve implantation of human cancer cell lines into the anatomically corresponding organ of immunodeficient mice to reproduce tumor growth within a native microenvironment, enabling more clinically relevant tumor behavior compared with subcutaneous models. These models are widely used because orthotopic placement better recapitulates tumor progression, including invasion and metastatic spread, which are often underrepresented in heterotopic implantation systems. Compared with conventional xenografts, orthotopic implantation is described as more technically complex but provides improved simulation of tumor-microenvironment interactions and metastatic behavior, making it particularly valuable for translational oncology research. Surgical orthotopic implantation approaches have been emphasized as enabling faithful reproduction of clinical cancer features, including metastasis and disease progression patterns that align with the tumor’s organ of origi
Pureza y Documentación
Referencias
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)