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galaking schreef op 7 oktober 2020 18:45 :
Start Phase 2: GLPG2737. Het lijkt me dat Galapagos hier zeker middels een persbericht aandacht aan had kunnen schenken
Misschien binnenkort als de eerste patient behandeld is?
GLPG2737 staat in de investor presentation overigens nog als PH1 program: www.glpg.com/docs/view/5f761fbab1628-... ,-12,17 Aangezien Galapagos zich hier toch op een nieuw ziektedomein richt zou het goed zijn als ze toch nog een PB maken met verdere toelichting op achtergrond en doel van deze studie.
Nieuw wetenschappelijk artikel (sep20) waar GLPG2737 wordt vermeld:www.sciencedirect.com/science/article... Potential therapeutic role of CFTR inhibitors in ADPKD “An exploratory, randomized, double-bling, placebo-controlled multicenter study evaluating the efficacy, safety, tolerability and pharmacokinetics of the orally administered CFTR corrector GLPG2737 in patients with ADPKD has been initiated recently (Galapagos; EudraCT2019–003521-21).”
In Spanje zijn blijkbaar 4 locaties voorzien:nomenclator.org/estudio-para-evaluar-... CENTERS CENTER 1: FUNDACIÓ PUIGVERT - IUNA NAME CENTRO FUNDACIÓ PUIGVERT - IUNA. LOCALITY CENTER Barcelona. PROVINCE BARCELONA. CATALONIA AUTONOMOUS COMMUNITY . Nephrology DEPARTMENT . STATUS Not started. INACTIVE DATE 06/30/2020. CENTER 2: UNIVERSITY HOSPITAL OCTOBER 12 NAME UNIVERSITY HOSPITAL CENTER OCTOBER 12. LOCALITY CENTER Madrid. MADRID PROVINCE . AUTONOMOUS COMMUNITY MADRID, COMMUNITY OF. Nephrology DEPARTMENT . STATUS Not started. INACTIVE DATE 06/30/2020. CENTER 3: HOSPITAL UNIVERSITARI DE BELLVITGE NAME CENTRO HOSPITAL UNIVERSITARI DE BELLVITGE. LOCALITY CENTER Hospitalet de Llobregat, L '. PROVINCE BARCELONA. CATALONIA AUTONOMOUS COMMUNITY . Nephrology DEPARTMENT . STATUS Not started. INACTIVE DATE 06/30/2020. CENTER 4: UNIVERSITY HOSPITAL DR. PESET ALEIXANDRE NAME CENTRO HOSPITAL UNIVERSITARIO DR. PESET ALEIXANDRE. LOCALITY CENTER Valencia. VALENCIA PROVINCE . COMUNITAT VALENCIANA AUTONOMOUS COMMUNITY. Nephrology DEPARTMENT . STATUS Not started. INACTIVE DATE 06/30/2020.
Lama Daila schreef op 7 oktober 2020 21:15 :
Nieuw wetenschappelijk artikel (sep20) waar GLPG2737 wordt vermeld:
www.sciencedirect.com/science/article... Potential therapeutic role of CFTR inhibitors in ADPKD
“An exploratory, randomized, double-bling, placebo-controlled multicenter study evaluating the efficacy, safety, tolerability and pharmacokinetics of the orally administered CFTR corrector
GLPG2737 in patients with ADPKD has been initiated recently (Galapagos; EudraCT2019–003521-21).”
Is er hier iemand die dit soort artikels kan begrijpen en er ons iets begrijpbaar kan over te vertellen? Lingus? Maxen? Of anderen?
Wat ik ervan begrijp is dat dezelfde CFTR- channels als in de longen ook in de nieren minder goed functioneren in het buiten de cel brengen van chloride-ionen en vloeistof. En dat je dat dus met soortgelijke moleculen/werkingsmechanismen zou kunnen aanpakken. Ben geen wetenschapper of deskundige, maar het leest op die manier. Zie in het plaatje trouwens ook ENAC staan, epithelial sodium channel. Dat is een target dat Arrowhead probeert aan te pakken met RNAi in Cystic Fibrose. Als dat lukt, kunnen ze hier wellicht ook aan werken.
TODAY 8 October 2020 18:00 - 19:00 CEST Live webinar with Dr Séverine Vermeire, Onno van de Stolpe and Dr Mark C. Genovese about IBD/UC. TWO TEAMS, ONE VISION, MULTIPLE DRUG CANDIDATE THERAPIES We’re committed to beating inflammatory disease, and our complementary strengths make us far more capable of doing so. Through our research and development efforts, we will relentlessly pursue novel therapies that break through the efficacy ceiling as we strive to improve the lives of patients living with IBD.Live Webinar – Thursday 8th October 2020. 18:00–19:00 (CEST) event.on24.com/eventRegistration/Even...
Wall Street Trader schreef op 8 oktober 2020 10:35 :
TODAY 8 October 2020 18:00 - 19:00 CEST Live webinar with Dr Séverine Vermeire, Onno van de Stolpe and Dr Mark C. Genovese about IBD/UC. TWO TEAMS, ONE VISION, MULTIPLE DRUG CANDIDATE THERAPIES
We’re committed to beating inflammatory disease, and our complementary strengths make us far more capable of doing so.
Through our research and development efforts, we will relentlessly pursue novel therapies that break through the efficacy ceiling as we strive to improve the lives of patients living with IBD.
Live Webinar – Thursday 8th October 2020. 18:00–19:00 (CEST) event.on24.com/eventRegistration/Even... Meer nieuws volgende week bij UEG meeting?. Onno was blij dat jij nog even Toledo kon noemen....
De voornaamste slides en boodschappen van deze webinar op deze twitter-collectie:twitter.com/lama_daila/status/1314264... Galapagos: webinar “UC The Future” $GLPG IBD: Innovate Build Discover Interesting webinar with @SeverineVermei1 @OvandeStolpe and Mark Genovese (Gilead) Mark en Onno explained their collaboration and commitment to IBD. Séverine Vermeire (KU Leuven) explained why innovation is still essential in UC and the how the JAK-STAT-pathway (selective JAK’s) are promising wrt the remaining considerable unmet needs $GLPG Next week on UEG week (Symposium Galapagos & Gilead on Monday October 12th) final results of the Selection Phase3 study (Filgotinib in UC) will be presented $GLPG Q&A: Toledo $GLPG Round Table on October 27th: great event! Data, targets, results preclinical trials 2 Phase2 studies started recently (SEA TURTLE, LADYBUG). 3 other Phase2 studies will be launched before end of year JAK inhibitors in IBD: promising in UC and CD $GLPG MD PhD Séverine Vermeire: Avoid JAK2. (Selective) JAK1, JAK3 and TYK2 are preferable. @SeverineVermei1 Collaboration Galapagos-Gilead: Addressing unmet needs in immune-mediated inflammatory diseases requires innovative approaches $GLPG How does the collaboration work? $GLPG $GILD It began with filgotinib $GLPG But we’re just getting started $GLPG JAK inhibitors reduce the activity of multiple cytokines implicated in IBD pathogenesis $GLPG Filgotinib: JAK1-preferential inhibitor $GLPG Full results of the SELECTION trial will be presented at UEG Week 2020 ! Webinar “UC the future” Thank you for attending $GLPG For more information on Gilead and Galapagos’ activities: UEG Week Virtual, including late breakers and the symposium
Summary of the Live webinar with Dr Séverine Vermeire, Onno van de Stolpe and Dr Mark C. Genovese about IBD/UC. Screenshots and summary thanks to Lama Daila!
Galapagos: 3 nieuwe patenten mbt IRAK-4: WO2020200898: patentscope.wipo.int/search/en/detail... WO2020200899: patentscope.wipo.int/search/en/detail... WO2020200900: patentscope.wipo.int/search/en/detail... NOVEL COMPOUNDS AND PHARMACEUTICAL COMPOSITIONS THEREOF FOR THE TREATMENT OF INFLAMMATORY DISORDERSen.wikipedia.org/wiki/IRAK4 IRAK-4 (interleukin-1 receptor-associated kinase 4), in the IRAK family, is a protein kinase involved in signaling innate immune responses from Toll-like receptors.
Heb op Toledo-draadje ook al eens Toll-like receptors als targets gesuggereerd. Ben benieuwd ... nog 2,5 weken.
Blijkbaar is er ook een relatie tussen TLR's en Interleukine-1. Ze vormen een superfamilie met 3 subgroepen. TLRs are a type of pattern recognition receptor (PRR) and recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). TLRs together with the Interleukin-1 receptors form a receptor superfamily, known as the "interleukin-1 receptor / toll-like receptor superfamily"; all members of this family have in common a so-called TIR (toll-IL-1 receptor) domain. Three subgroups of TIR domains exist. Proteins with subgroup 1 TIR domains are receptors for interleukins that are produced by macrophages, monocytes, and dendritic cells and all have extracellular Immunoglobulin (Ig) domains. Proteins with subgroup 2 TIR domains are classical TLRs, and bind directly or indirectly to molecules of microbial origin. A third subgroup of proteins containing TIR domains consists of adaptor proteins that are exclusively cytosolic and mediate signaling from proteins of subgroups 1 and 2. After ligand binding, the first step of IL-1R family signalling is oligomerization of TIR domains present on receptors (IL-1R, TLR), coreceptors (IL-1R accessory protein, CD14) and adaptor molecules (MyD88). TIR domain present on receptor creates a heterodimer with TIR domain on accessory protein. This high affinity receptor complex recruits downstream signalling molecules. The signal is transduced by cytoplasmatic kinases (such as IRAKs) and by other adaptors, such as tumor necrosis factor 6 (TRAF6). The final step of signalization is phosphorilation of the inhibitory molecule IkB by IkB kinase complex leading to transcription factor NF-?B releasing. NF-?B is translocated into nucleus and by binding DNA intermediates inflammatory, alergic and non-alergic immune response.[6] Type I IL-1R (IL-1RI) also known as CD121a is receptor for IL-1a, IL-1ß and IL-1RA. IL-1RI signalling is involved in thymocyte proliferation, B cells development, IL-2 and IL-6 production, stress responses, inflammatory responses, sleep regulation and appetite.[2] IL-1RI signalling plays also important role in Th17 development.[7][8] Studies of human autoimmune diseases such as sclerosis multiplex, Rheumatoid arthritis, psoriasis or autoimmune inflammatory bowel diseases show that defect in IL-1R1 signalling is responsible for Th17-mediated autoimmune diseases.[9] IL-1R signalling is regulated by negative regulators such as inhibitory IL-R1 type II (IL-1RII), soluble IL-1RI and sIL-RII and IL-1Ra.[10] It can be also regulated on the level of downstream signalling molecules by inhibiting recruitment of IRAKs, or by suppression of MyD88 secretion. IL-1R cooperates with receptor accessory protein and both are expressed on T cells, fibroblasts and endothelial cells.[10]en.wikipedia.org/wiki/Toll-like_receptor en.wikipedia.org/wiki/Toll-Interleuki... en.wikipedia.org/wiki/Interleukin-1_r... Geen idee of het relevant is, ik ben een leek die wat stukjes informatie bij elkaar gooit. Slaat misschien nergens op.
Nog even verder gekeken, die receptor lijkt 2 vormen te hebben, pro-inflammatoir (zie post hierboven die type 1 effect in o.a. RA aangeeft) en anti-inflammatoir. Interleukin-1 receptor (IL-1R) is a cytokine receptor which binds interleukin 1.[1] Two forms of the receptor exist. The type I receptor is primarily responsible for transmitting the inflammatory effects of interleukin-1 (IL-1) while type II receptors may act as a suppressor of IL-1 activity by competing for IL-1 binding.[1] Also opposing the effects of IL-1 is the IL-1 receptor antagonist (IL-1RA).[2] Wat als je een molecuul hebt dat die receptor van de ene naar de andere vorm kan switchen? En dus de balans tussen die pro en die anti kan beïnvloeden?
Sunday marks the first day of virtual UEG Week. IBD needs innovation as many patients continue to suffer debilitating symptoms. Read how we are relentlessly pursuing new treatment approaches as we work to improve lives of patients with IBD:www.glpg.com/our-story/story-overview... Professor Vermeire, from the Gastroenterology Department of the University Hospital Leuven shares her insights on the impact of this disease on young people below. www.youtube.com/watch?v=eAMdsbeyd1g "We go after the diseases that some companies may shy away from because the chances of success seem low. We trust our science and our biology, and we go after targets that we think we can make a big difference to the quality of patients’ lives. I am excited by what the future will bring as we continue to share our scientific knowledge and goals to develop medicines that change the course of disease for UC patients." Dr. Walid Abi-Saab, Chief Medical Officer at Galapagos
Driven by new therapies, the Crohn’s disease market will experience significant growth during the next decade 9 October 2020 Crohn’s disease is a form of inflammatory bowel disease (IBD), which is composed of two chronic autoimmune diseases that cause intestinal inflammation: Crohn’s disease and ulcerative colitis (UC). In Crohn’s disease, chronic inflammation may affect any part of the gastrointestinal (GI) tract from the mouth to the anal area; however, the disease occurs most commonly in the lower part of the small intestine (ileum) and in the large intestine. The pathophysiology of Crohn’s disease is complex, as the disease is characterised by recurring flares that evolve along with periods of inactivity and remission. The Crohn’s disease market has historically been reliant on anti-tumour necrosis factor (anti-TNF) therapies that have been available for over a decade, but recent developments have led to research on novel mechanisms of action (MOAs) in order to combat the high numbers of patients experiencing treatment non-response. The Crohn’s disease market will experience significant growth due mainly to the launch of new drugs, most of which are expected to launch between 2023–2025, that will target the moderate-to-severe patient population, as well as the often-neglected patient with fistulising disease.Most notable are the IL-23 inhibitors , which are suspected to offer greater efficacy and safety than Stelara, and include AbbVie’s Skyrizi (risankizumab), Janssen’s Tremfya (guselkumab), Eli Lilly’s mirikizumab, and AstraZeneca’s brazikumab. Similarly anticipated are the Janus kinase (JAK) inhibitors, which include AbbVie’s Rinvoq (upadacitinib) and Gilead’s Jyseleca (filgotinib) . Article continues below: www.pharmaceutical-technology.com/com...
Lama Daila schreef op 7 oktober 2020 17:49 :
Zouden we een apart draadje moeten openen voor GLPG2737 voor ADPKD ?
Hier nog wat info dat ik in mei al op het inhoudelijk draadje gezet had:
Met dank aan Sanderus die deze Europese trial toen al had ontdekt:
www.clinicaltrialsregister.eu/ctr-sea... twitter.com/lama_daila/status/1260299... GLPG2737 Autosomal dominant polycystic kidney disease
Filmpje op YouTube:
www.youtube.com/watch?v=dShs9-XSemI Rarediseases info:
rarediseases.info.nih.gov/diseases/10... Piet2010:
Dit is toch wel bijzonder. GLPG2737 staat in het Q1 verslag als een klinische kandidaat met een nieuw, nog niet bekend gemaakt werkingsmechanisme. En nu blijkt het te gaan om een nierziekte die ik overigens zelf heb. Had GLPG hier niet een persbericht over uit kunnen/moeten geven ?
Ik heb het nieuwe draadje geopend. Voel je vrij om het verder aan te vullen.
Summary of the Bolero online biotechevent - zaterdag 10 oktober 2020 Screenshots and summary thanks to Lama Daila!
Wall Street Trader schreef op 10 oktober 2020 14:07 :
Summary of the Bolero online biotechevent - zaterdag 10 oktober 2020 Screenshots and summary thanks to Lama Daila!
Thanks WST. Thumbs up! And Lama obviously!
holenbeer schreef op 9 oktober 2020 08:57 :
Blijkbaar is er ook een relatie tussen TLR's en Interleukine-1. Ze vormen een superfamilie met 3 subgroepen.
Mooi opzoekwerk holenbeer. Hier gooi je echter 2 dingen bij elkaar die niet op deze manier bij elkaar horen. Cellulaire reactiepaden kan je versimpeld zien als rijtjes dominostenen die klaar staan om aangetikt te worden, waarna een serie reacties volgt, als omvallende dominostenen. In deze beeldspraak zijn interleukines de vingers die de reactie aantikken en de receptors (TLR's en IL-R's) zijn de eerste dominosteen in een serie. Die eerste dominostenen staan in het celmemraan te wachten op activatie. Interleukines (een van de vele cytokines) zijn in deze beeldspraak de aantikvingers, TLR's en IL-R's (receptoren) zijn de wachtende eerste dominostenen. De cascade aan reacties (de volgende dominostenen) gebeurt vaak in de cel en kunnen weer andere reacties triggeren, waaronder reacties die aan het einde van de rij dominostenen het DNA aansporen om bepaalde eiwitten te maken via de route DNA-uitlezing, RNA-productie, eiwitproductie. Cytokines (waaronder interleukines) zijn geen familie van receptoren (waaronder TLR's en IL-R's). Ze werken wel samen. Wat uitleg over Toll Like Receptors, zie www.youtube.com/watch?v=8mEnyBdsrr8 enwww.youtube.com/watch?v=yM4kIC_DfEg Uit deze video's begrijp ik dat de TLR's en de IL-R's (beide receptorfamilies) in het intracellulaire gedeelte aardig overeenkomen en in het extracellulaire gedeelte verschillen. Vandaar dus superfamilie. Een beetje diepere duik in die materie:www.ncbi.nlm.nih.gov/pmc/articles/PMC... (deze moet ik zelf ook nog doorlezen, dus ik ben wel blij met een regenachtig weekend. Ik zag de welbekende SIK's ook genoemd in dit document uit 2014, kan dus om meerdere redenen interessant leesvoer zijn). Terzijde: De TLR’s zijn evolutionair zeer oud; ze komen voor in bacteriën, planten en zoogdieren, met lichte variaties. De TLR’s werden al sinds de eerste helft van de vorige eeuw vermoed, maar pas in 1985 ontdekt in de fruitvlieg. De curieuze naam is afkomstig van de uitroep van één van de ontdekkers, Christian Nüsslein-Volhard: “Das ist ja toll!” De celbiologie excelleert in curieuze naamgeving en hetzelfde component heeft soms wel drie, vier, vijf verschillende namen en afkortingen – wen er maar aan.
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VendexKBB
VEON
Vermogensbeheer
Versatel
VESTAS WIND SYSTEMS
VGP
Via Net.Works
Viohalco
Vivendi
Vivoryon Therapeutics
VNU
VolkerWessels
Volkswagen
Volta Finance
Vonovia
Vopak
Warehouses
Wave Life Sciences Ltd
Wavin
WDP
Wegener
Weibo Corp
Wereldhave
Wereldhave Belgium
Wessanen
What's Cooking
Wolters Kluwer
X-FAB
Xebec
Xeikon
Xior
Yatra Capital Limited
Zalando
Zenitel
Zénobe Gramme
Ziggo
Zilver - Silver World Spot (USD)