2. Immunology/Inflammation Apoptosis PI3K/Akt/mTOR
  3. MHC Apoptosis IFNAR TNF Receptor Interleukin Related Akt mTOR
  4. Anti-CD160 Antibody (MAT 302)

Anti-CD160 Antibody (MAT 302)  (Synonyms: CL1-R2)

Cat. No.: HY-P992201
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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.

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Anti-CD160 Antibody (MAT 302)

Anti-CD160 Antibody (MAT 302) Chemical Structure

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Anti-CD160 Antibody (MAT 302) Related Antibodies

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Description

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[1][2][3][4].

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.

Anti-CD160 Antibody (MAT 302) Related Antibodies

Apoptosis Analysis[4]

Cell Line: human umbilical vein endothelial cells (HUVECs), primary human fibroblasts
Concentration: 10 μg/mL
Incubation Time: 50 h
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.

Apoptosis Analysis[4]

Cell Line: human umbilical vein endothelial cells (HUVECs), SGHEC-7 endothelial cells
Concentration: 1 μg/mL, 10 μg/mL
Incubation Time: up to 50 h
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) (25-100 μg; subconjunctival injection; 2 administrations for early/combination/monotherapy regimens, 2 administrations for late-stage regimen, and 1 administration for Fab'2 regimen) significantly inhibits corneal neovascularization (CNV) induced by FGF2 and VEGF in rabbits. It exerts a synergistic effect when combined with Bevacizumab (HY-P9906), and early treatment reduces CNV grading by up to 73%[1].
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.

Animal Model: Rabbit[1]
Dosage: 25 μg (monotherapy); 50 μg (monotherapy); 100 μg (early treatment; late treatment); 100 μg CL1-R2 Fab'2
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)
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.
Animal Model: C57BL/6J (7 days old)[2]
Dosage: 5 µg per eye
Administration: i.v.i.; single injection on postnatal day 12
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.
Animal Model: BALB/c (7-10 weeks old)[2]
Dosage: 25 µg per plug; 200 µg per injection
Administration: incorporated into Matrigel at implantation; direct plug injection; every other day for 7 days
Result: Reduced hemoglobin content in Matrigel plugs by ~45%.
Showed smaller, fewer vessels in CL1-R2-treated plugs via histological analysis.
Animal Model: C57BL/6 (7-10 weeks old)[2]
Dosage: 500 µg per injection
Administration: i.p.; three times per week starting on tumor inoculation day
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

11126  [NCBI]

Accession

O95971
Target

CD160
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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Anti-CD160 Antibody (MAT 302) 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:

Anti-CD160 Antibody (MAT 302)CL1-R2MHCApoptosisIFNARTNF ReceptorInterleukin RelatedAktmTORMajor Histocompatibility ComplexInterferon-α/β receptorInterferon-alpha/beta receptor Tumor Necrosis Factor ReceptorTNFRILPKBProtein kinase BMammalian target of RapamycinNK cellsendothelial cellCD160FGF2Lewis lung carcinomaHVEMAKT/mTOR/s6k signalingmelanomahuman umbilical vein endothelial cellsHIV infectionInhibitorinhibitorinhibit

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