BI-1607
BI-1607 is a humanized monoclonal antibody targeting FcγRIIB/CD32b. BI-1607 selectively blocks inhibitory FcγRIIB signaling, abrogates its inhibitory function, redirects tumor cell-bound antibodies to activating FcγRs, and its modified Fc region prevents the binding of its own Fc segment to FcγRs. BI-1607 reduces αPD-1 trogocytosis, enhances the effector functions of anti-tumor antibodies (including ADCP and ADCC, promotes intratumoral regulatory T cell (Treg) depletion, myeloid cell reprogramming, induction of interferon-γ (IFN-γ) and CXCL10, and increases the number of activated effector CD8+ T cells. BI-1607 can be used in research related to colorectal cancer, HER2-positive advanced solid tumors, HER2-positive locally advanced or metastatic breast cancer, and HER2-positive metastatic gastric cancer.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
Biologische Aktivität
Human
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FcγRIIB |
CD32b |
αPD-1 |
IFN-γ |
CXCL10 |
BI-1607 (20 μg/mL; 30-60 min) reduces αPD-1 trogocytosis from PD-1-expressing Jurkat cells to human monocyte-derived macrophages[1].
BI-1607 increases the activating-to-inhibitory FcγR ratio on human monocyte-derived macrophages via selective FcγRIIB blockade[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
BI-1607 (10 mg/kg; i.v.; single dose) does not induce significant in vivo B-cell depletion in human FcγRIIB transgenic mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:B-hCTLA-4 (6-8 week-old, female, 17-20 grams, subcutaneous inoculation of MC38 cells)[1]
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Dosage:10 mg/kg (in combination with 1 mg/kg ipilimumab)
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Administration:i.p.; 3 times on days 1, 4, and 8
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Result:Significantly improved survival compared to ipilimumab alone or BI-1607 alone.
Elevated serum and tumor levels of TNF-α, IFN-γ, and CXCL10 compared to ipilimumab alone.
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Animal Model:hFcγRIIB ± x mFcγRII-/- C57BL/6[2]
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Dosage:10 mg/kg
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Administration:i.v.; single dose
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Result:Showed no significant depletion of B cells 48 hours after administration, compared with pretreatment levels.
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Unconjugated
The product can be reconstituted/diluted with sterile PBS or saline.
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Product Image
ELISA, FACS, Functional assay
Chemical Information
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SMILES
N/A
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Oldham RJ, et al. Tailored FcγR blockade enhances immune checkpoint therapy and overcomes resistance. Journal of experimental & clinical cancer research : CR. 2026 Jul 25;45(1):167. [Content Brief]
[2]. Cortés J, et al. A First-in-Class mAb (BI-1607) Targeting FcγRIIB: Preclinical Data and First-in-Human Studies in Patients with HER2-Positive Advanced Solid Tumors. Clinical cancer research : an official journal of the American Association for Cancer Research. 2025 Dec 01;31(23):4953-4963. [Content Brief]
[5]. Yasuda T, et al. Gastric cancer immunosuppressive microenvironment heterogeneity: implications for therapy development. Trends Cancer. 2024 Jul;10(7):627-642. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
BI-1607 Related Classifications
HY-P991582 Related Classifications
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- BI-1607
- BI1607
- BI 1607
- Fc Receptor (FcR)
- IFNAR
- PD-1/PD-L1
- CXCR
- colon adenocarcinoma
- ADCP
- ADCC
- colorectal cancer
- HER2-positive metastatic gastric or gastroesophageal junction adenocarcinoma
- gastric cancer
- HER2-positive advanced solid tumors
- FcγRIIB
- HER2-positive locally advanced or metastatic breast cancer
- CD32b
- Inhibitor
- inhibitor
- inhibit