Anti-Human IL13 Recombinant Antibody (Tralokinumab) (CAT#: TAB-218)

Figure 1 Tralokinumab prevents IL-13 from interacting with both (a) IL-13Rα1 and (b) IL-13Rα2.

Data are shown as mean % DeltaF (standard error of the mean) from two independent experiments each performed in duplicate.

Popovic, B., Breed, J., Rees, D. G., Gardener, M. J., Vinall, L. M. K., Kemp, B., ... & Colice, G. (2017). Structural characterisation reveals mechanism of IL-13-neutralising monoclonal antibody tralokinumab as inhibition of binding to IL-13Rα1 and IL-13Rα2. Journal of molecular biology, 429(2), 208-219.

Figure 2 Overall structure of the tralokinumab:IL-13 complex.

Heavy chain (VH) is coloured in dark blue, light chain (VL) is coloured in light blue, and IL-13 is shown in purple. Helices A–D of IL-13 are also labelled.

Popovic, B., Breed, J., Rees, D. G., Gardener, M. J., Vinall, L. M. K., Kemp, B., ... & Colice, G. (2017). Structural characterisation reveals mechanism of IL-13-neutralising monoclonal antibody tralokinumab as inhibition of binding to IL-13Rα1 and IL-13Rα2. Journal of molecular biology, 429(2), 208-219.

Figure 3 Neutralization of fibroblast-derived IL-13 inhibits lung fibrosis in an established fibroblast-driven disease setting in humanized SCID mice.

(A–C)Isolated IPF fibroblasts (n= 5) or normal lung tissue fibroblasts (n= 5) were injected intravenously to SCID mice, and animals were killed at specificsubsequent time points. Whole lung mRNA expression was measured by quantitative RT-PCR for il-13 (A), il113ra1(B), and il-13ra2(C) and normalized tolung mRNA expression levels from mice that had received normal lung tissue-derived fibroblasts. (D–N) Thirty-five days after IPF fibroblast engraftment,mice were randomized and treated with PBS control, control IgG4, or tralokinumab (anti–IL-13 mAb) every other day until analysis at Day 63.Representative mouse lung sections stained with Masson's trichrome to depict the degree of fibrosis at Day 63 from SCID/IPF mice treated with PBScontrol (D), CAT251 IgG4isotype control (E), and tralokinumab anti–IL-13 antibody (F). Fibrosis was quantitated in all animals using a modifiedAshcroft score of histological sections (G). Tralokinumab attenuated serum CC16 levels as measured by ELISA (H) and BAL caspase 3 activity (I). Data aremean 6SEM (n= 5). (J–M) Representative immunohistochemistry localizing IL-13Ra2 expression in the lungs of control SCID mice that have notreceived IPF fibroblast (J) or SCID/IPF mice treated with PBS control (K), isotype control (L), or tralokinumab (M). Original magnification: top panels,340;bottom panels,3200. *p<0.05, **p<0.01, and ***p<0.005.

Murray, L. A., Zhang, H., Oak, S. R., Coelho, A. L., Herath, A., Flaherty, K. R., ... & Sleeman, M. A. (2014). Targeting interleukin-13 with tralokinumab attenuates lung fibrosis and epithelial damage in a humanized SCID idiopathic pulmonary fibrosis model. American journal of respiratory cell and molecular biology, 50(5), 985-994.

Figure 4 Enhanced epithelial markers in the lungs of SCID/IPF mice treated with tralokinumab.

Whole lung mRNA expression from mice treated withisotype control or tralokinumab (anti–IL-13) was measured using quantitative RT-PCR. Levels of vimentin (A), TGF-b1(B), surfactant protein a (C),surfactant protein b (D), surfactant protein c (E), surfactant protein d (F), and e-cadherin (G) were quantitated and normalized to lung mRNA expressionlevels from SCID/IPF mice that had received PBS control only. Data are mean 6SEM (n= 5). *p<0.05.

Murray, L. A., Zhang, H., Oak, S. R., Coelho, A. L., Herath, A., Flaherty, K. R., ... & Sleeman, M. A. (2014). Targeting interleukin-13 with tralokinumab attenuates lung fibrosis and epithelial damage in a humanized SCID idiopathic pulmonary fibrosis model. American journal of respiratory cell and molecular biology, 50(5), 985-994.

Figure 1 Anti-Human IL13 Antibody (Tralokinumab) (TAB-218) in ELISA

ELISA analysis of TAB-218 was performed by coating with Recombinant Human IL3.