BI-836880
BI-836880 is a humanized bispecific nanobody and a selective inhibitor of VEGF and ANG2, with a Kd of 16 pM for hANG2, an EC50 of 1.4 nM for VEGF165, and an EC50 of 2.3 nM for VEGF121. BI-836880 blocks ERK phosphorylation downstream of VEGF-A as well as TIE2 phosphorylation downstream of ANG2. BI-836880 does not inhibit ANG1-mediated TIE2 phosphorylation. BI-836880 exerts anti-angiogenic effects, reduces the number of immature endothelial vessels in tumor tissues, and inhibits tumor growth in preclinical models. BI-836880 can be used in the research of pancreatic cancer, non-small cell lung cancer, renal cell carcinoma, ovarian cancer, colon cancer, and Lewis lung cancer.
For research use only. We do not sell to patients.
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Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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All VEGFR Isoforms
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Biological Activity
VHH-VHH-VHH
Human
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Tie2 |
BI-836880 (0.4-500 nM) binds potently and selectively to hANG2 (KD = 16 pM) and serum albumin (KD = 9 nM) in cell-free surface plasmon resonance assays[1].
BI-836880 binds selectively to hVEGF-A (EC50 = 1.4 nM for VEGF165, 2.3 nM for VEGF121), and no binding to other VEGF family members or placental growth factor is detected in cell-free ELISA assays[1].
BI-836880 potently blocks the binding of hANG2-TIE2 (IC50 = 45-50 pM) and shows no activity against ANG1-TIE2 binding in cell-free assays[1].
BI-836880 (0.16-20 nM; 5 min) potently inhibits VEGF-induced phosphorylation of ERK in human umbilical vein endothelial cells (HUVECs), with an IC50 of 1.1-1.4 nM and an inhibition rate of 84-93%[1].
BI-836880 (0.04-10.42 nM; 3 days) potently inhibits VEGF-induced proliferation of human umbilical vein endothelial cells (HUVEC), with an IC50 of 0.6-0.8 nM and an inhibition rate of 84-93%[1].
BI-836880 (following a 15-minute incubation) potently inhibits ANG2-induced TIE2 phosphorylation in TIE2-transfected HEK293 cells, with an IC50 of 1.3-3.2 nM, and shows no activity against ANG1-induced TIE2 phosphorylation[1].
BI-836880 (at log M concentrations ranging from -11 to -6; 72 h) completely inhibits ANG2-induced HUVEC survival in real-time impedance analysis, with an IC50 of 1.9 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:0.16-20 nM
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Incubation Time:5 min
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Result:Inhibited VEGF-induced ERK phosphorylation by 93% with an IC50 of 1.1 nM in the absence of HSA.
Inhibited VEGF-induced ERK phosphorylation by 84% with an IC50 of 1.4 nM in the presence of HSA.
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Cell Line:human umbilical vein endothelial cells (HUVECs)
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Concentration:0.04-10.42 nM
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Incubation Time:3 days
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Result:Inhibited VEGF-induced HUVEC proliferation by 84% with an IC50 of 0.8 nM in the absence of HSA.
Inhibited VEGF-induced HUVEC proliferation by 93% with an IC50 of 0.6 nM in the presence of HSA.
BI-836880 (15 mg/kg; i.p.; twice weekly; days 4 to 30) induces a 27% tumor growth inhibition (TGI) in the LL/2 syngeneic tumor model. Its combination with anti-PD-1 and VEGFR2 inhibition strategies increases TGI to 80%, while delaying tumor growth, improving tumor immune cell infiltration and promoting vascular normalization[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NMRI-Foxn1nu (female)[1]
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Dosage:13.7 mg/kg
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Administration:i.p.; twice weekly; 2.5-9 weeks
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Result:Induced tumor growth inhibition (TGI) ranging from 51% (renal cell cancer model RXF 1220) to 92% (breast cancer model MAXF 401).
Showed significantly greater TGI than bevacizumab in seven of eleven models (PAXF 546, PAXF 736, PAXF 1872, LXFE 211, LXFE 1422, RXF 1220, MAXF 1322).
Showed significantly greater TGI than AMG386 in two models (PAXF 546, LXFE 1422).
Caused no body weight loss or deaths in most models; in cachexia-inducing models, no additional body weight loss linked to treatment compared to control and bevacizumab groups.
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Animal Model:C57BL/6NTac (female)[1]
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Dosage:15 mg/kg
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Administration:i.p.; twice weekly; day 4 to day 30
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Result:Induced a TGI of 27% as monotherapy.
When combined with anti-PD-1 antibody RMP1-14, reached a TGI of 48%.
When added to the combination of RMP1-14 and vatalanib, reached a TGI of 80%, with a trend toward reduced tumor volumes (17% smaller on day 26) and delayed time for tumors to reach 500 mm3 compared to RMP1-14 plus vatalanib alone.
Reduced endothelial immature vessel numbers and CD31 mRNA expression in tumor tissue as monotherapy.
When combined with vatalanib and RMP1-14, showed a trend toward increased CD3-positive T-cell density in tumors.
VEGFA & Ang2/ANGPT2/Angiopoietin2
Unconjugated
The product can be reconstituted/diluted with sterile PBS or saline.
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ELISA, FACS, Functional assay
Chemical Information
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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