Inhaled JAK inhibitor GDC-0214 reduces exhaled nitric oxide in patients with mild asthma: A randomized, controlled, proof-of-activity trial.


Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
09 2021
Historique:
received: 11 11 2020
revised: 01 02 2021
accepted: 23 02 2021
pubmed: 22 3 2021
medline: 11 11 2021
entrez: 21 3 2021
Statut: ppublish

Résumé

The Janus kinase (JAK) pathway mediates the activity of many asthma-relevant cytokines, including IL-4 and IL-13. GDC-0214 is a potent, inhaled, small-molecule JAK inhibitor being developed for the treatment of asthma. We sought to determine whether GDC-0214 reduces fractional exhaled nitric oxide (Feno), a JAK1-dependent biomarker of airway inflammation, in patients with mild asthma. We conducted a double-blind, randomized, placebo-controlled, phase 1 proof-of-activity study in adults with mild asthma and Feno higher than 40 parts per billion (ppb). Subjects were randomized 2:1 (GDC-0214:placebo) into 4 sequential ascending-dose cohorts (1 mg once daily [QD], 4 mg QD, 15 mg QD, or 15 mg twice daily). All subjects received 4 days of blinded placebo, then 10 days of either active drug or placebo. The primary outcome was placebo-corrected percent reduction in Feno from baseline to day 14. Baseline was defined as the average Feno during the blinded placebo period. Pharmacokinetics, safety, and tolerability were also assessed. Thirty-six subjects (mean age, 28 years; 54% females) were enrolled. Mean Feno at baseline across all subjects was 93 ± 43 ppb. At day 14, placebo-corrected difference in Feno was -23% (95% CI, -37.3 to -9) for 15 mg QD and -42% (95% CI, -57 to -27.4) for 15 mg twice daily. Higher plasma exposure was associated with greater Feno reduction. No dose-limiting adverse events, serious adverse events, or treatment discontinuations occurred. There were no major imbalances in adverse events or laboratory findings, or evidence of systemic JAK inhibition. GDC-0214, an inhaled JAK inhibitor, caused dose-dependent reductions in Feno in mild asthma and was well tolerated without evidence of systemic toxicity.

Sections du résumé

BACKGROUND
The Janus kinase (JAK) pathway mediates the activity of many asthma-relevant cytokines, including IL-4 and IL-13. GDC-0214 is a potent, inhaled, small-molecule JAK inhibitor being developed for the treatment of asthma.
OBJECTIVE
We sought to determine whether GDC-0214 reduces fractional exhaled nitric oxide (Feno), a JAK1-dependent biomarker of airway inflammation, in patients with mild asthma.
METHODS
We conducted a double-blind, randomized, placebo-controlled, phase 1 proof-of-activity study in adults with mild asthma and Feno higher than 40 parts per billion (ppb). Subjects were randomized 2:1 (GDC-0214:placebo) into 4 sequential ascending-dose cohorts (1 mg once daily [QD], 4 mg QD, 15 mg QD, or 15 mg twice daily). All subjects received 4 days of blinded placebo, then 10 days of either active drug or placebo. The primary outcome was placebo-corrected percent reduction in Feno from baseline to day 14. Baseline was defined as the average Feno during the blinded placebo period. Pharmacokinetics, safety, and tolerability were also assessed.
RESULTS
Thirty-six subjects (mean age, 28 years; 54% females) were enrolled. Mean Feno at baseline across all subjects was 93 ± 43 ppb. At day 14, placebo-corrected difference in Feno was -23% (95% CI, -37.3 to -9) for 15 mg QD and -42% (95% CI, -57 to -27.4) for 15 mg twice daily. Higher plasma exposure was associated with greater Feno reduction. No dose-limiting adverse events, serious adverse events, or treatment discontinuations occurred. There were no major imbalances in adverse events or laboratory findings, or evidence of systemic JAK inhibition.
CONCLUSIONS
GDC-0214, an inhaled JAK inhibitor, caused dose-dependent reductions in Feno in mild asthma and was well tolerated without evidence of systemic toxicity.

Identifiants

pubmed: 33744327
pii: S0091-6749(21)00422-X
doi: 10.1016/j.jaci.2021.02.042
pii:
doi:

Substances chimiques

Anti-Asthmatic Agents 0
Janus Kinase Inhibitors 0
Nitric Oxide 31C4KY9ESH

Types de publication

Clinical Trial, Phase I Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

783-789

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Irene E Braithwaite (IE)

Medical Research Institute of New Zealand, Wellington, New Zealand. Electronic address: irene.braithwaite@mrinz.ac.nz.

Fang Cai (F)

Genentech, Inc, South San Francisco, Calif.

Jennifer A Tom (JA)

Genentech, Inc, South San Francisco, Calif.

Joshua M Galanter (JM)

Genentech, Inc, South San Francisco, Calif.

Ryan P Owen (RP)

Genentech, Inc, South San Francisco, Calif.

Rui Zhu (R)

Genentech, Inc, South San Francisco, Calif.

Mathew Williams (M)

Medical Research Institute of New Zealand, Wellington, New Zealand.

Anna G McGregor (AG)

Genentech, Inc, South San Francisco, Calif.

Avi Eliahu (A)

Genentech, Inc, South San Francisco, Calif.

Matthew R Durk (MR)

Genentech, Inc, South San Francisco, Calif.

Hart S Dengler (HS)

Genentech, Inc, South San Francisco, Calif.

Mark Zak (M)

Genentech, Inc, South San Francisco, Calif.

Jane R Kenny (JR)

Genentech, Inc, South San Francisco, Calif.

Maria E Wilson (ME)

Genentech, Inc, South San Francisco, Calif.

Richard Beasley (R)

Medical Research Institute of New Zealand, Wellington, New Zealand.

Hubert Chen (H)

Genentech, Inc, South San Francisco, Calif.

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Classifications MeSH