Pharmacological suppression of the kallikrein kinin system with KVD900: An orally available plasma kallikrein inhibitor for the on-demand treatment of hereditary angioedema.


Journal

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
ISSN: 1365-2222
Titre abrégé: Clin Exp Allergy
Pays: England
ID NLM: 8906443

Informations de publication

Date de publication:
09 2022
Historique:
revised: 02 02 2022
received: 08 11 2021
accepted: 01 03 2022
pubmed: 13 3 2022
medline: 1 9 2022
entrez: 12 3 2022
Statut: ppublish

Résumé

Hereditary angioedema (HAE) is a rare genetic disease that leads to recurrent episodes of swelling and pain caused by uncontrolled plasma kallikrein (PKa) activity. Current guidelines recommend ready availability of on-demand HAE treatments that can be administered early upon attack onset. This report describes the pharmacological and pharmacodynamic properties of the novel oral small-molecule PKa inhibitor KVD900 as a potential on-demand treatment for HAE. Pharmacological properties of KVD900 on PKa and closely related serine proteases were characterized using kinetic fluorogenic substrate activity assays. Effects of KVD900 on PKa activity and kallikrein kinin system activation in whole plasma were measured in the presence of dextran sulphate (DXS)-stimulation using a fluorogenic substrate and capillary immunoassays to quantify high molecular weight kininogen (HK), plasma prekallikrein and Factor XII cleavage. Pharmacodynamic effects of orally administered KVD900 were characterized in plasma samples from six healthy controls in a first in human phase 1 clinical trial and from 12 participants with HAE in a phase 2 clinical trial. KVD900 is a selective, competitive and reversible inhibitor of human PKa enzyme with a K KVD900 is a fast-acting oral PKa inhibitor that rapidly inhibits PKa activity, kallikrein kinin system activation and HK cleavage in plasma. On-demand administration of KVD900 may provide an opportunity to halt the generation of bradykinin and reverse HAE attacks.

Sections du résumé

BACKGROUND
Hereditary angioedema (HAE) is a rare genetic disease that leads to recurrent episodes of swelling and pain caused by uncontrolled plasma kallikrein (PKa) activity. Current guidelines recommend ready availability of on-demand HAE treatments that can be administered early upon attack onset. This report describes the pharmacological and pharmacodynamic properties of the novel oral small-molecule PKa inhibitor KVD900 as a potential on-demand treatment for HAE.
METHODS
Pharmacological properties of KVD900 on PKa and closely related serine proteases were characterized using kinetic fluorogenic substrate activity assays. Effects of KVD900 on PKa activity and kallikrein kinin system activation in whole plasma were measured in the presence of dextran sulphate (DXS)-stimulation using a fluorogenic substrate and capillary immunoassays to quantify high molecular weight kininogen (HK), plasma prekallikrein and Factor XII cleavage. Pharmacodynamic effects of orally administered KVD900 were characterized in plasma samples from six healthy controls in a first in human phase 1 clinical trial and from 12 participants with HAE in a phase 2 clinical trial.
RESULTS
KVD900 is a selective, competitive and reversible inhibitor of human PKa enzyme with a K
CONCLUSION
KVD900 is a fast-acting oral PKa inhibitor that rapidly inhibits PKa activity, kallikrein kinin system activation and HK cleavage in plasma. On-demand administration of KVD900 may provide an opportunity to halt the generation of bradykinin and reverse HAE attacks.

Identifiants

pubmed: 35278245
doi: 10.1111/cea.14122
pmc: PMC9544254
doi:

Substances chimiques

Complement C1 Inhibitor Protein 0
Fluorescent Dyes 0
Factor XII 9001-30-3
Prekallikrein 9055-02-1
Plasma Kallikrein EC 3.4.21.34
Bradykinin S8TIM42R2W

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1059-1070

Informations de copyright

© 2022 KalVista Pharmaceuticals, Inc. Clinical & Experimental Allergy published by John Wiley & Sons Ltd.

Références

Am J Med. 2006 Mar;119(3):267-74
pubmed: 16490473
Arch Intern Med. 2003 May 26;163(10):1229-35
pubmed: 12767961
N Engl J Med. 2010 Aug 5;363(6):513-22
pubmed: 20818886
Allergy. 2018 Aug;73(8):1575-1596
pubmed: 29318628
J Allergy Clin Immunol. 2022 Jun;149(6):2034-2042
pubmed: 35086692
Ann Allergy Asthma Immunol. 2013 Sep;111(3):211-5
pubmed: 23987198
Invest Ophthalmol Vis Sci. 2021 Sep 2;62(12):15
pubmed: 34533563
Immunol Allergy Clin North Am. 2017 Aug;37(3):513-525
pubmed: 28687106
J Allergy Clin Immunol. 2017 Dec;140(6):1700-1703.e8
pubmed: 28782632
Clin Exp Allergy. 2014 Dec;44(12):1503-14
pubmed: 24552232
J Allergy Clin Immunol Pract. 2021 Jan;9(1):132-150.e3
pubmed: 32898710
J Allergy Clin Immunol. 2011 Jul;128(1):153-159.e4
pubmed: 21481442
Int Immunopharmacol. 2008 Feb;8(2):276-81
pubmed: 18182240
Lancet. 2012 Feb 4;379(9814):474-81
pubmed: 22305226
J Innate Immun. 2018;10(2):94-105
pubmed: 29237166
Clin Rev Allergy Immunol. 2021 Aug;61(1):66-76
pubmed: 33423210
Biochim Biophys Acta Mol Cell Res. 2017 Nov;1864(11 Pt B):2118-2127
pubmed: 28743596
Clin Exp Allergy. 2022 Sep;52(9):1059-1070
pubmed: 35278245
J Clin Chem Clin Biochem. 1988 Jul;26(7):423-7
pubmed: 3146615
N Engl J Med. 2010 Aug 5;363(6):532-41
pubmed: 20818888
Front Med (Lausanne). 2018 Jan 25;5:3
pubmed: 29423395
Thromb Res. 2016 Apr;140:118-124
pubmed: 26950760
J Allergy Clin Immunol. 2009 Oct;124(4):801-8
pubmed: 19767078
N Engl J Med. 2017 Feb 23;376(8):717-728
pubmed: 28225674
FASEB J. 2019 Feb;33(2):2599-2609
pubmed: 30281335
J Clin Med. 2021 May 09;10(9):
pubmed: 34065094
J Pharmacol Exp Ther. 2000 Jul;294(1):263-9
pubmed: 10871321
N Engl J Med. 1983 May 5;308(18):1050-3
pubmed: 6601240
Allergy Asthma Proc. 2011 Jul-Aug;32(4):319-24
pubmed: 21781409
Blood. 2017 Mar 16;129(11):1527-1537
pubmed: 28069606
Chem Immunol Allergy. 2014;100:205-13
pubmed: 24925400
Hum Mutat. 2020 Jan;41(1):38-57
pubmed: 31517426
Blood. 1991 Jun 15;77(12):2660-7
pubmed: 1710516
Orphanet J Rare Dis. 2018 May 4;13(1):73
pubmed: 29728119
Biochemistry. 1993 Nov 16;32(45):12136-47
pubmed: 7692967
Biochem Pharmacol. 1975 Dec 1;24(23):2177-85
pubmed: 1212266

Auteurs

Edward J Duckworth (EJ)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Nivetha Murugesan (N)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Lily Li (L)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Louise J Rushbrooke (LJ)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Daniel K Lee (DK)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Gian Marco De Donatis (GM)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Andreas Maetzel (A)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.
Institute for Health Policy, Management & Evaluation, University of Toronto, Toronto, Ontario, Canada.

Christopher M Yea (CM)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Sally L Hampton (SL)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Edward P Feener (EP)

KalVista Pharmaceuticals, Cambridge, Massachusetts, USA.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH