Cosentyx immunogenicity low in psoriasis patients

[Fred]

This study investigated the immunogenicity of Cosentyx (secukinumab) across six phase III clinical trials in patients with plaque psoriasis were treated with for up to 52 weeks and additionally followed up at week 60.

Quote:

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Background:
The proinflammatory cytokine interleukin (IL)-17A plays a pivotal role in psoriasis pathogenesis. Secukinumab, a fully human monoclonal antibody (mAb) that selectively targets IL-17A, has been demonstrated to be highly efficacious for the treatment of moderate-to-severe psoriasis, starting at early time points, with a sustained effect and a favourable safety profile. mAb therapies may be associated with production of antidrug antibodies (ADAs) that can affect drug pharmacokinetics, diminish response or cause hypersensitivity reactions.

Objectives:
To investigate the immunogenicity of secukinumab across six phase III clinical trials in which patients with plaque psoriasis were treated with secukinumab for up to 52 weeks and additionally followed up at week 60.

Methods:
Immunogenicity in patients with plaque psoriasis exposed to secukinumab was evaluated at baseline and at weeks 12, 24, 52 and 60. Treatment-emergent (TE)-ADAs were defined as a positive ADA signal detected in post-treatment samples from patients with a negative baseline signal. Confirmed positive samples were further analysed for their drug-neutralizing potential.

Results:
Among 2842 patients receiving secukinumab and evaluated for ADAs, 11 (0·4%) developed TE-ADAs. Associations between TE-ADAs and secukinumab dose, frequency or mode of administration were not observed. Neutralizing antibodies were detected in three of nine evaluable patients with TE-ADAs.

Conclusions:
Secukinumab immunogenicity was low, as shown by TE-ADA detection in only 11 of 2842 (0·4%) patients with moderate-to-severe plaque psoriasis treated with secukinumab. All but one of the patients with TE-ADAs were biologic naive. Neither TE-ADAs nor neutralizing antibodies were associated with loss of secukinumab efficacy or issues of clinical concern.

Source: onlinelibrary.wiley.com

*Funding: Novartis

Cosentyx (secukinumab)

[Caroline]

Ehhhh, this is good right?

[Fred]

Ehhhh, this is good right?

Yes. I can see your thinking, but it means the way I read it (and I'll stand corrected if I'm wrong) only 11 people from 2842 built up a reject if you like against Cosentyx.

Sort of like I was thinking I had done with Stelara, my body had become used to it over time and it was no longer working as well as it was when I first started.

I think that's the way to explain it.

[mataribot]

Drug antibodies or whatever you want to call them are more closely related to side  effects than failure to respond.

[Fred]

Drug antibodies or whatever you want to call them are more closely related to side  effects than failure to respond.

So it means there were only 11 from 2842 that experienced side effects?

[mataribot]

There is a posative correlation between drug antibodies and drug induced autoimmune diseases such as lupus. It does not imply that people who have an SE have a high test AB test results. Sorry if I did not make that clear in the first post.

The idea that people who have high drug AB will fail treatment is theory - one where there are many counter examples.

[Fred]

There is a posative correlation between drug antibodies and drug induced autoimmune diseases such as lupus. It does not imply that people who have an SE have a high test AB test results. Sorry if I did not make that clear in the first post.

The idea that people who have high drug AB will fail treatment is theory - one where there are many counter examples.

No it wasn't that you weren't clear. I didn't quiet understand, and to be honest I still don't.

Sorry Matari I'm just not getting it.