Anti-Human IL17A Recombinant Antibody (Bimekizumab) (CAT#: TAB-H08)

Figure 1 IL-17F expression was observed in tissue biopsies from patients with PsA.

Suppression of neutrophil and monocyte (Fig.) migration was substantially greater with bimekizumab than with blockade of IL-17A alone.

Maroof, A., Okoye, R., Smallie, T., Baeten, D., Archer, S., Simpson, C.,... & Shaw, S. (2017). THU0038 Bimekizumab dual inhibition of IL-17A and IL-17F provides evidence of IL-17F contribution to chronic inflammation in disease-relevant cells.

Figure 2 IL-17F contributes to inflammation and bimekizumab demonstrates superior efficacy relative to inhibition of IL-17A or IL-17F alone.

Recombinant IL-17A and IL-17F, with or without TNF, were used to activate either (A) PsA synoviocytes (n=2) or (B) NHDFs (n=4), and IL-8 release was assessed following overnight culture. To evaluate the individual and collective influence of IL-17A and IL-17F, (C) PsA synoviocytes (n=4), (D, F, G) primary NHDFs (n=4) or (E) normal synoviocytes (n=5) were stimulated with Th17 supernatant with or without IL-17-specific blocking antibodies. Following overnight culture, either (C, D) inhibition of IL-8 production, (E, F) gene transcriptional changes or (G) inhibition of chemotactic potential was evaluated. For transcriptional analysis (E, F), genes were normalised to GAPDH mRNA and expressed as relative fold changes compared with unstimulated cells. For primary NHDFs, the panel presents genes that had a fold change ≥3 for Th17 stimulation under IgG conditions.

Glatt, S., Baeten, D., Baker, T., Griffiths, M., Ionescu, L., Lawson, A. D.,... & Vajjah, P. (2018). Dual IL-17A and IL-17F neutralisation by bimekizumab in psoriatic arthritis: evidence from preclinical experiments and a randomised placebo-controlled clinical trial that IL-17F contributes to human chronic tissue inflammation. Annals of the rheumatic diseases, 77(4), 523-532.

Figure 3 Pharmacokinetic parameters of bimekizumab (PK-PPS).

(A) GeoMean plasma concentration–time profile of bimekizumab (PK-PPS) and (B) table of pharmacokinetic variables of bimekizumab. PK-PPS, pharmacokinetic per-protocol set. Note: Means, SDs and CVs were only calculated if at least one-third of the concentrations were quantified at a respective time point. CV, coefficient of variation.

Glatt, S., Baeten, D., Baker, T., Griffiths, M., Ionescu, L., Lawson, A. D.,... & Vajjah, P. (2018). Dual IL-17A and IL-17F neutralisation by bimekizumab in psoriatic arthritis: evidence from preclinical experiments and a randomised placebo-controlled clinical trial that IL-17F contributes to human chronic tissue inflammation. Annals of the rheumatic diseases, 77(4), 523-532.

Figure 4 ACR and PASI response rates by treatment group (PD-PPS).

(A–C) ACR response rates (%, with 95% CI) and (D-E) PASI response rates (%, with 95% CI). Dashed vertical lines indicate drug intake (weeks 0, 3 and 6).

Glatt, S., Baeten, D., Baker, T., Griffiths, M., Ionescu, L., Lawson, A. D.,... & Vajjah, P. (2018). Dual IL-17A and IL-17F neutralisation by bimekizumab in psoriatic arthritis: evidence from preclinical experiments and a randomised placebo-controlled clinical trial that IL-17F contributes to human chronic tissue inflammation. Annals of the rheumatic diseases, 77(4), 523-532.

Figure 5 Dose proportionality (pharmacokinetic per-protocol set): individual area under the curve (AUC) vs. bimekizumab dose.

Note: at bimekizumab 480 mg, the AUC was reported for five subjects. The AUC was not calculated for one subject because insufficient data points were available in the elimination phase of the pharmacokinetic profile.

Glatt, S., Helmer, E., Haier, B., Strimenopoulou, F., Price, G., Vajjah, P.,... & Shaw, S. (2017). First‐in‐human randomized study of bimekizumab, a humanized monoclonal antibody and selective dual inhibitor of IL‐17A and IL‐17F, in mild psoriasis. British journal of clinical pharmacology, 83(5), 991-1001.

Figure 1 Anti-Human IL17A Recombinant Antibody (TAB-H08) in ELISA

ELISA analysis of TAB-H08 was performed by coating with human IL17A protein (His tag). Then blocked with BSA and incubated with TAB-H08. The HRP-conjugated goat anti-IgG was used as a secondary antibody (1: 2000). Detection was performed using TMB substrate and stopped with sulfuric acid. The absorbances were read on a spectrophotometer at 450 nm.

Figure 2 Anti-Human IL17A Recombinant Antibody (TAB-H08) in WB

Western blot analysis of TAB-H08 was performed by loading human IL17A protein onto a 12% Tris-HCl polyacrylamide gel. Proteins were transferred to a CN membrane and blocked with 5% skim milk for at least one hour. Membranes were probed with TAB-H08 and a HRP goat anti-IgG (H+L) was used as the secondary antibody (1: 3000). Chemiluminescent detection was performed.

Figure 3 Anti-Human IL17A Recombinant Antibody (TAB-H08) in DB

Dot Blot analysis of TAB-H08 was performed by coating with human IL17A protein (His tag).

TAB-H08 incubation concentration: 2 μg/mL.
HRP-conjugated goat anti- IgG (H+L) secondary antibody (1: 3000)
NC: Negative control, PC: Positive control