Entyvio 300mg Powder for Concentrate for Solution for Infusion

Land: Malaysia

Sprog: engelsk

Kilde: NPRA (National Pharmaceutical Regulatory Agency, Bahagian Regulatori Farmasi Negara)

Aktiv bestanddel:

Vedolizumab

Tilgængelig fra:

Takeda Malaysia Sdn Bhd

INN (International Name):

Vedolizumab

Enheder i pakken:

20mL x 1vial Vials

Fremstillet af:

Takeda Austria GmbH

Indlægsseddel

NOT APPLICABLE

Produktets egenskaber

1
NAME OF THE MEDICINAL PRODUCT
Entyvio 300mg, powder for concentrate for solution for infusion.
NAME AND STRENGTH OF ACTIVE SUBSTANCES
Each vial contains 300 mg of vedolizumab.
After reconstitution, each mL contains 60 mg of vedolizumab.
Excipients: _L-histidine, L-histidine monohydrochloride, L-arginine
hydrochloride, sucrose, polysorbate 80. _
_ _
_ _
PRODUCT DESCRIPTION
Entyvio powder for concentrate for solution for infusion is supplied
as white to off-white lyophilized cake or powder.
CLINICAL PHARMACOLOGY
Pharmacologic class: selective immunosuppressants
ATC code: L04AA33
Pharmacotherapeutic group: immunosuppressants
MECHANISM OF ACTION
VedolizumabEntyvio is a gut-selective immunosuppressive biologic. It
is a humanized monoclonal antibody that
binds specifically to the α4β7 integrin, which is preferentially
expressed on gut-homing T helper lymphocytes. By
binding to α4β7 on certain lymphocytes, vedolizumab inhibits
adhesion of these cells to mucosal addressin cell
adhesion molecule-1 (MAdCAM-1), but not to vascular cell adhesion
molecule-1 (VCAM-1). MAdCAM-1 is mainly
expressed on gut endothelial cells and plays a critical role in the
homing of T lymphocytes to tissues within the
gastrointestinal tract. Vedolizumab does not bind to, nor inhibit
function of, the α4β1 and αEβ7 integrins.
The α4β7 integrin is expressed on a discrete subset of memory T
helper lymphocytes which preferentially migrate
into the gastrointestinal (GI) tract and cause inflammation that is
characteristic of ulcerative colitis and Crohn’s
disease, both of which are chronic, inflammatory,
immunologically-mediated conditions of the GI tract. Vedolizumab
reduces GI inflammation in UC patients. Inhibiting the interaction of
α4β7 with MAdCAM-1 with vedolizumab prevents
transmigration of gut-homing memory T helper lymphocytes across the
vascular endothelium into parenchymal
tissue in non-human primates and induced a reversible 3-fold elevation
of these cells in peripheral blood. The murine
precursor of vedolizumab alleviated G