Anti-CD160 Antibody (MAT 302)
Based on 1 Customer Validation
Anti-CD160 Antibody (MAT 302) (CL1-R2) is a human monoclonal antibody targeting CD160. Anti-CD160 Antibody (MAT 302) blocks the CD160-HVEM protein interaction, inhibits FGF2-mediated renal tubular vascular growth, and induces endothelial cell apoptosis. Anti-CD160 Antibody (MAT 302) targets CD160 on neovascularization to exert anti-angiogenic and vascular normalization effects, trigger the production of IFN-γ, TNF and IL-6 by NK cells, and enhance glucose metabolism of NK cells through the AKT/mTOR/s6k signaling pathway. Anti-CD160 Antibody (MAT 302) reduces vascular density, normalizes remaining tumor blood vessels, and inhibits tumor growth in melanoma-bearing mice. Anti-CD160 Antibody (MAT 302) can be used in research related to neovascularization, proliferative diabetic retinopathy, and melanoma.
For research use only. We do not sell to patients.
- Purity : 97.32%
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Species Reactivity
Human
IC50 & Target
[3]|
IL-6 |
In Vitro
Anti-CD160 Antibody (MAT 302) inhibits FGF2-mediated tubular angiogenesis in CD160-expressing human umbilical vein endothelial cells[1].
Anti-CD160 Antibody (MAT 302) inhibits FGF2-mediated tubule formation and induces apoptosis in CD160-expressing human umbilical vein endothelial cells[2].
Anti-CD160 Antibody (MAT 302) (6 µg/mL) specifically binds to CD160 expressed on neovascular endothelial cells of human colon cancer[2].
Anti-CD160 Antibody (MAT 302) (10 µg/mL; 1-h pre-incubation followed by 24-hour cytokine stimulation) significantly enhances the production of IFN-γ and GLUT1 in total NK cells infected with HIV[3].
Anti-CD160 Antibody (MAT 302) (10 µg/mL; 30-minute incubation) activates the PI3K/AKT/mTOR/s6k signaling pathway in total NK cells infected with HIV, and significantly increases the phosphorylation levels of AKT, mTOR and s6k[3].
Anti-CD160 Antibody (MAT 302) (1-10 μg/mL; 24 h) inhibits FGF2-induced capillary tube formation in human umbilical vein endothelial cells (HUVECs)[4].
Anti-CD160 Antibody (MAT 302) (10 μg/mL; 50 h) induces apoptosis in HUVEC in the presence of VEGF, but does not induce apoptosis in primary human fibroblasts[4].
Anti-CD160 Antibody (MAT 302) (1-10 μg/mL; 0-50 h) induces time-dependent apoptosis in HUVECs and SGHEC-7 endothelial cells[4].
Anti-CD160 Antibody (MAT 302) (20 μg/mL; 2 h at 4°C) binds to HUVEC and HMVEC[4].
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), primary human fibroblasts
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Concentration:10 μg/mL
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Incubation Time:50 h
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Result:Induced apoptosis in HUVECs, resulting in a percentage of annexin V-positive cells comparable to sHLA-G1 treatment.
Showed no significant apoptosis induction in primary human fibroblasts.
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Cell Line:human umbilical vein endothelial cells (HUVECs), SGHEC-7 endothelial cells
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Concentration:1 μg/mL, 10 μg/mL
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Incubation Time:up to 50 h
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Result:Induced time-dependent apoptosis in HUVECs and SGHEC-7 cells, with apoptotic morphology (cytoplasmic/nuclear shrinkage, phase-bright appearance, membrane blebbing) observed over the 50-hour monitoring period.
In Vivo
Anti-CD160 Antibody (MAT 302) (5 µg per eye; intravitreal injection; single injection on postnatal day 12) effectively inhibits pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy, reducing endothelial cell nuclei by approximately 35% and vascular lumens by approximately 50% compared with the control group[2].
Anti-CD160 Antibody (MAT 302) (25 µg per plug, mixed with Matrigel during implantation; 200 µg per injection, directly injected into the plug, once every 2 days for 7 days) significantly inhibits FGF2-induced neovascularization in the mouse Matrigel plug assay, reducing hemoglobin content by approximately 45% compared with the control group[2].
Combination treatment with Anti-CD160 Antibody (MAT 302) (500 µg per injection; intraperitoneal injection; three times per week starting from the day of tumor inoculation) and Cyclophosphamide (HY-17420) reduces the vascular density of B16 melanoma by approximately 40%, normalizes the remaining tumor blood vessels, enhances drug delivery, significantly inhibits tumor growth in mice, and improves their survival outcomes[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rabbit[1]
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Dosage:25 μg (monotherapy); 50 μg (monotherapy); 100 μg (early treatment; late treatment); 100 μg CL1-R2 Fab'2
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Administration:subconjunctival; two injections (day 1 and day 3 for early treatment/combination/25-100 μg monotherapy); two injections (day 6 and day 8 for late treatment); single injection (CL1-R2 Fab'2)
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Result:Reduced CNV grades by 53% (FGF2-induced) and 73% (VEGF-induced) with early 100 μg treatment compared to control IgG.
Reduced CNV grades by 57.32% with late 100 μg treatment compared to control IgG, with 45% reduction in neovessel area.
Reduced CNV by 25% with 25 μg monotherapy.
Showed equivalent potency to matching doses of bevacizumab with 50 μg and 100 μg monotherapy.
Produced additive antiangiogenic effects when combined with 25 μg bevacizumab, with increased CNV inhibition as CL1-R2 dose increased.
Inhibited CNV to a similar extent as whole CL1-R2 IgG and bevacizumab with CL1-R2 Fab'2.
Reduced corneal neovascular invasion and decreased endothelial cell proliferation (Ki-67 staining) compared to control.
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Animal Model:C57BL/6J (7 days old)[2]
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Dosage:5 µg per eye
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Administration:i.v.i.; single injection on postnatal day 12
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Result:Decreased the mean number of endothelial cell nuclei per section by ~35%.
Reduced the mean number of vessel lumens per section by ~50%.
Reduced avascular area, neovascular tufts, and tortuous/dilated radial vessels in flat-mounted retinas.
Decreased aberrant microvessels in retinal histology sections.
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Animal Model:BALB/c (7-10 weeks old)[2]
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Dosage:25 µg per plug; 200 µg per injection
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Administration:incorporated into Matrigel at implantation; direct plug injection; every other day for 7 days
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Result:Reduced hemoglobin content in Matrigel plugs by ~45%.
Showed smaller, fewer vessels in CL1-R2-treated plugs via histological analysis.
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Animal Model:C57BL/6 (7-10 weeks old)[2]
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Dosage:500 µg per injection
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Administration:i.p.; three times per week starting on tumor inoculation day
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Result:Reduced B16 tumor vascular density by ~40% compared with control IgG1 plus cyclophosphamide.
Showed significantly fewer intratumoral vessels at days 12, 15, and 18 post-injection.
Reduced tumor vascular area by 2.56-fold at day 14 post-implantation.
Reduced vessel fractal dimension, indicating improved hierarchical architecture.
Increased the proportion of vessels with open lumens by ~60%.
Increased pericyte coverage by >200%.
Increased perfused vessels by ~166%.
Increased tumor necrosis by ~114%.
Significantly reduced tumor growth.
Improved mouse survival to 35 days, compared with 30 days for bevacizumab or control IgG1-treated mice.
Gene ID
Accession
O95971
Target
CD160
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
ELISA, FACS, Functional assay
Chemical Information
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Appearance Liquid
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Color Colorless to light yellow
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Synonyms
CL1-R2
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Shipping
Shipping with dry ice.
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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
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Data Sheet (272 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
[1]. Menguy T, et al. Anti-CD160, Alone or in Combination With Bevacizumab, Is a Potent Inhibitor of Ocular Neovascularization in Rabbit and Monkey Models. Invest Ophthalmol Vis Sci. 2018;59(7):2687-2698. [Content Brief]
[2]. Chabot S, et al. A novel antiangiogenic and vascular normalization therapy targeted against human CD160 receptor. J Exp Med. 2011 May 9;208(5):973-86. [Content Brief]
[3]. Sun Z, et al. CD160 Promotes NK Cell Functions by Upregulating Glucose Metabolism and Negatively Correlates With HIV Disease Progression. Front Immunol. 2022;13:854432. Published 2022 Aug 19. [Content Brief]
[4]. Fons P, et al. Soluble HLA-G1 inhibits angiogenesis through an apoptotic pathway and by direct binding to CD160 receptor expressed by endothelial cells. Blood. 2006;108(8):2608-2615. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Anti-CD160 Antibody (MAT 302) Related Classifications
HY-P992201 Related Classifications
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