Anti-VEGFC ADCC Enhanced Antibody (VGX100) is an ADCC enhanced antibody produced by our Afuco™ platform. VGX-100 is a human antibody that acts against the human vascular endothelial growth factor (VEGF)-C protein. Treatment for cancers, particularly glioblastoma and metastatic colorectal cancers, are the first target indications for VGX-100. Additionally, VGX-100 is developing for a number of other cancer indications, and as an agent to treat front-of the-eye diseases.
Figure 1 Corneal blood and lymphatic vessel growth are suppressed by VEGF-C blockade.
(A) Fluorescent microscopic images (×40 magnification) of immunohistochemical staining of flat-mount corneas reveal reduced densities of blood and lymphatic vessels in anti-VEGF-C-treated mice. Growth of the vessels can be seen from the limbal area toward the sutures. (B) Quantitative comparison demonstrates significant reductions in the percentage of total corneal area covered by blood and lymphatic vessels after VEGF-C blockade. Graphs represent mean ± SEM of 10 mice in each group. *P < 0.05, **P < 0.01.
Hajrasouliha, A. R., Funaki, T., Sadrai, Z., Hattori, T., Chauhan, S. K., & Dana, R. (2012). Vascular endothelial growth factor-C promotes alloimmunity by amplifying antigen-presenting cell maturation and lymphangiogenesis.Investigative ophthalmology & visual science, 53(3), 1244-1250.
Figure 2 Trafficking of APCs to draining lymph nodes after corneal transplantation is suppressed by anti-VEGF-C.
Percentage of CD11b+ APCs in ipsilateral draining lymph nodes of transplanted corneas evaluated at different time points (days 1, 3, 7, and 14 post-transplant) by flow cytometry. APC content of the draining lymph nodes is significantly increased at day 1 after transplantation and returns to normal levels by day 3. Administration of anti-VEGF-C antibody significantly blocked the early rise in the APC content of draining lymph nodes. Results represent mean ± SEM of five samples per group (**P < 0.01 compared with control).
Hajrasouliha, A. R., Funaki, T., Sadrai, Z., Hattori, T., Chauhan, S. K., & Dana, R. (2012). Vascular endothelial growth factor-C promotes alloimmunity by amplifying antigen-presenting cell maturation and lymphangiogenesis.Investigative ophthalmology & visual science, 53(3), 1244-1250.
Figure 3 VEGF-C promotes DC maturation.
(A, B) Recipient (Iad) and donor (Iab) APCs from ipsilateral draining lymph nodes express significantly lower levels of MHC class II after anti-VEGF-C blockade (day 1 to day 3 after corneal transplantation. Anti-VEGF-C administration significantly reduced MHC class II expression by both donor and recipient after transplantation. (C) Bone marrow-derived DCs were matured either by LPS alone or LPS in the presence of 10 ng/mL VEGF-C for 24 hours. LPS-induced DC maturation was associated with overexpression of MHC class II, which was augmented in the presence of VEGF-C. Data are representative of three different experiments.
Hajrasouliha, A. R., Funaki, T., Sadrai, Z., Hattori, T., Chauhan, S. K., & Dana, R. (2012). Vascular endothelial growth factor-C promotes alloimmunity by amplifying antigen-presenting cell maturation and lymphangiogenesis.Investigative ophthalmology & visual science, 53(3), 1244-1250.
Figure 4 VEGF-C blockade promotes corneal allotransplant survival.
In a masked fashion, orthotopically transplanted corneas from C57BL/6 (Iaᵇ) to BALB/c (Iaᵈ) mice were examined biomicroscopically and scored using a grading system designed to detect rejection for 8 weeks after transplantation. The fate of corneal graft is reported by Kaplan-Meier survival curves. VEGF-C blockade reduced the graft rejection rate and markedly improved graft survival from 33% in the control group to 66% in the anti-VEGF-C-treated group (n = 20 per group; *P < 0.05).
Hajrasouliha, A. R., Funaki, T., Sadrai, Z., Hattori, T., Chauhan, S. K., & Dana, R. (2012). Vascular endothelial growth factor-C promotes alloimmunity by amplifying antigen-presenting cell maturation and lymphangiogenesis.Investigative ophthalmology & visual science, 53(3), 1244-1250.
Figure 5 VEGFC-targeted therapy in AML.
A, VEGFC protein expression analysis using ELISA on NBM (n = 4) cells, CD34− AML cells (n = 3), and CD34+ AML cells (n = 5). Flow cytometry KDR (VEGFR-2) membrane protein expression levels of pediatric AML blasts (n = 60) and NBM (n = 5) controls. FLT4 (VEGFR-3) membrane protein expression levels on pediatric AML blasts (n = 18) and NBM (n = 5) controls. Box plots show the median, and error bars define data distribution. B, VEGFC targeting study approach to identify the molecular mechanism of action. C, May-Grunwald-Giemsa staining of THP-1 cells in the presence or absence of VEGFC-targeting human antibody (30 μg/mL). D, CD11b and CD14 membrane protein expression by flow cytometric analysis of THP-1-untreated and anti-VEGFC-treated cells (mean ± SEM). E, Flow cytometric dose-dependent apoptosis analysis of anti-VEGFC-treated THP-1 cells using Annexin V staining (mean ± SEM). F, Flow cytometric KDR membrane protein expression analysis upon VEGFC-targeting antibody treatment in THP-1 cells (mean ± SEM). Statistical analysis: *, P < 0.05.
Kampen, K. R., Scherpen, F. J., Mahmud, H., ter Elst, A., Mulder, A. B., Guryev, V.,... & De Bont, E. S. (2018). VEGFC antibody therapy drives differentiation of AML. Cancer research, 78(20), 5940-5948.
Figure 6 VEGFC-targeting therapy effects on CD34+ AML stem and progenitor cells.
A, CFC assay analysis of CD34+ pediatric AML cells using a single dose of VEGFC antibody treatment representing the number CFC colonies (left) and the total CFC cell counts (right; n = 6). B, CD34+ AML expansion potential in LTC-IC assay after 7 weeks of AML culturing on a mouse stromal feeder layer (n = 7). C, CD34+ AML expansion potential of cobblestone-forming cells residing underneath the stromal layer after 5 weeks of culturing, measured in limiting dilutions by their CFC output potential (n = 5). D, CFC, LTC-IC, and LTC-IC in limiting dilution represented per AML patient sample. E, Representative May-Grunwald-Giemsa-stained cytospins of untreated VEGFC antibody-treated CD34+ AML samples in CFC and LTC-IC assays. F, Microscopic quantification of AML cell culture composition after LTC-IC assays analysis comparing untreated and anti-VEGFC-treated cultures (n = 7). G, Box plot presenting the mean percentage of myelomonocytic cells quantified from May-Grunwald-Giemsa-stained cytospins comparing untreated and anti-VEGFC-treated cultures. H, Flow cytometry confirmation of anti-VEGFC-induced myelomonocytic differentiation in CD34+ AML CFC and LTC-IC assays by CD38, CD34, CD11b, and CD14 membrane protein expression analysis. I, Flow cytometric Annexin V/PI apoptosis analysis of untreated and anti-VEGFC-treated CD34+ AML CFC and LTC-IC cultures. All box plots represent the median, and error bars define data distribution. Statistical analysis: *, P < 0.05.
Kampen, K. R., Scherpen, F. J., Mahmud, H., ter Elst, A., Mulder, A. B., Guryev, V.,... & De Bont, E. S. (2018). VEGFC antibody therapy drives differentiation of AML. Cancer research, 78(20), 5940-5948.
Figure 7 Identification of anti-VEGFC-targeting mechanisms in pediatric AML and potential bypass mechanism.
A, Phosphoprotein array analysis presented as VEGFC antibody targeting effects relative to untreated control CD34+ AML samples (n = 3; mean ± SEM). B, Immunoblot confirmation of anti-VEGFC treatment effects on MAPK/Erk, and STAT5 protein expression and phosphorylation in pediatric CD34+ AML samples, CD34+ NBM controls, and THP-1 cells. Left, immunoblots. Right, combined quantification of the presented immunoblots. Box plots show the median, and error bars define data distribution. C, Flow cytometry VEGFC and KDR protein expression analysis combined with RPPA array analysis in CD34+ pediatric AML samples. The Venn diagram shows significantly overlapping protein expression. Bold proteins show a positive correlation, and nonbold proteins presented a negative correlation. All shown proteins were analyzed by RPPA analysis except the ones that are described to be analyzed by flow cytometry. D, FOXO3A immunoblot analysis of THP-1 cells treated for 72 hours with anti-VEGFC. Intracellular protein expression as measured by flow cytometry analysis of 24-hour anti-VEGFC-treated primary AML samples and THP-1 cells. E, Scrambled control vector and FOXO3A constitutive overexpressing THP-1 cells in the presence or absence of VEGFC antibody treatment analyzed for CD11b membrane protein expression levels measured using flow cytometry analysis (mean ± SEM). Statistical analysis: *, P < 0.05.
Kampen, K. R., Scherpen, F. J., Mahmud, H., ter Elst, A., Mulder, A. B., Guryev, V.,... & De Bont, E. S. (2018). VEGFC antibody therapy drives differentiation of AML. Cancer research, 78(20), 5940-5948.
Figure 8 VEGFC antibody therapy induced differentiation in a primary AML-xenografted animal model.
A, The WBC counts in the peripheral blood of mice injected with a primary EVI1 ASXL1 AML sample comparing DMSO with VEGFC antibody-treated animals. B and D, Histologic analysis was performed on bone marrow and spleens of disease progressed animals using a semiquantitative scoring system, e.g., 0 = no infiltration, 1 < 25% infiltration, 2 = 25%-75% infiltration, and 3> 75% infiltration. DMSO-treated animals were compared with VEGFC antibody-treated animals. B, Left, box plot presents the AML blast infiltration in the bone marrow. Right, box plot shows the infiltration of the AML-derived eosinophilic compartment in bone marrow. C, The box plot represents flow cytometric analysis showing the percentage of human CD11b membrane protein expression in the bone marrow of the AML-xenografted mice with on the right side the flow cytometry plots of the individual mice. D, Left, spleen lengths. Middle, histologic analysis of the AML blast infiltration in the spleen. Right, AML-derived eosinophilic compartment in the spleen. All box plots represent the median, and error bars define data distribution. Statistical analysis: *, P < 0.05.
Kampen, K. R., Scherpen, F. J., Mahmud, H., ter Elst, A., Mulder, A. B., Guryev, V.,... & De Bont, E. S. (2018). VEGFC antibody therapy drives differentiation of AML. Cancer research, 78(20), 5940-5948.
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CAT | Product Name | Application | Type |
---|---|---|---|
MOB-1722z | Mouse Anti-VEGFC Recombinant Antibody (clone 10F5) | WB, ICC, IF, IHC | Mouse IgG2a |
MOB-0226MC | Anti-Human VEGF-C Antibody | WB, ICC/IF, IHC, IHC-P | |
MOB-2183MZ | Recombinant Mouse Anti-Human VEGFC Antibody (clone 0/F8) | IHC-Fr, WB | Mouse antibody |
MRO-2271-CN | Rabbit Anti-VEGFC Polyclonal Antibody (MRO-2271-CN) | WB, IF, IHC, FC | Rabbit IgG |
VS3-CJ994 | Mouse Anti-VEGFC Recombinant Antibody (VS3-CJ994) | WB | Mouse IgG1, κ |
CAT | Product Name | Application | Type |
---|---|---|---|
TAB-661CL | Human Anti-VEGFC Recombinant Antibody (TAB-661CL) | ELISA | Human IgG |
TAB-311CQ | Human Anti-VEGFC Recombinant Antibody (TAB-311CQ) | ELISA, WB | Human IgG |
TAB-311CQ-S(P) | Human Anti-VEGFC Recombinant Antibody (TAB-311CQ-S(P)); scFv Fragment | ELISA, WB, Neut | Human scFv |
TAB-311CQ-F(E) | Human Anti-VEGFC Recombinant Antibody (TAB-311CQ-F(E)); Fab Fragment | ELISA, WB, Neut | Human Fab |
CAT | Product Name | Application | Type |
---|---|---|---|
TAB-309CQ | Human Anti-VEGFC Recombinant Antibody (TAB-309CQ) | Block, ELISA, FuncS | Humanized antibody |
TAB-309CQ-S(P) | Human Anti-VEGFC Recombinant Antibody; scFv Fragment (TAB-309CQ-S(P)) | ELISA, FC, WB, BL | Humanized scFv |
TAB-309CQ-F(E) | Human Anti-VEGFC Recombinant Antibody; Fab Fragment (TAB-309CQ-F(E)) | ELISA, FC, WB, BL | Humanized Fab |
CAT | Product Name | Application | Type |
---|---|---|---|
TAB-310CQ | Mouse Anti-VEGFC Recombinant Antibody (TAB-310CQ) | Block, ELISA, FuncS | Mouse IgG2a, κ |
TAB-310CQ-S(P) | Mouse Anti-VEGFC Recombinant Antibody; scFv Fragment (TAB-310CQ-S(P)) | ELISA, FC, WB, BL | Mouse scFv |
TAB-310CQ-F(E) | Mouse Anti-VEGFC Recombinant Antibody; Fab Fragment (TAB-310CQ-F(E)) | ELISA, FC, WB, BL | Mouse Fab |
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