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Filgotinib (GLPG-0634)

Alias: GLPG-0634; PubChemSID 163643231; GLPG0634; 1206101-20-3; Filgotinib; GLPG0634; 1206161-97-8; N-(5-(4-((1,1-dioxidothiomorpholino)methyl)phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl)cyclopropanecarboxamide; Filgotinib (GLPG0634); N-[5-[4-[(1,1-dioxo-1,4-thiazinan-4-yl)methyl]phenyl]-[1,2,4]triazolo[1,5-a]pyridin-2-yl]cyclopropanecarboxamide; GLPG 0634; Filgotinib
Cat No.:V0326 Purity: ≥98%
Filgotinib (also known as GLPG0634; GLPG-0634;Jyseleca) is a novel, potent and selective JAK1 (Janus kinase) inhibitor with potential anti-inflammatory activity.
Filgotinib (GLPG-0634)
Filgotinib (GLPG-0634) Chemical Structure CAS No.: 1206161-97-8
Product category: JAK
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Filgotinib (GLPG-0634):

  • GLPG0634 analogue
  • Filgotinib maleate
  • Filgotinib-d4
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Filgotinib (also known as GLPG0634; GLPG-0634; Jyseleca) is a novel, potent and selective JAK1 (Janus kinase) inhibitor with potential anti-inflammatory activity. As of 2020, it was approved as a medication for the treatment of rheumatoid arthritis. Filgotinib inhibits JAK1, JAK2, JAK3, and TYK2 with IC50 values of 10 nM, 28 nM, 810 nM, and 116 nM, respectively. It is currently being investigated for the treatment of rheumatoid arthritis (RA) and Crohn's disease. It is considered to be a promising drug candidate for treating autoimmune diseases by selectively inhibiting JAK1. In cellular assays, GLPG0634 is most potent in inhibiting the JAK1/JAK3/γc signaling induced by IL-2– and IL-4 as well as the JAK1/TYK2 type II receptor signaling induced by IFN-αB2. However, it shows lower potent to inhibit JAK2 homodimer–mediated signaling induced by EPO or PRL. In addition, GLPG0634 is found to inhibit the phosphorylation of STAT1 and STAT5 induced by cytokines.

Biological Activity I Assay Protocols (From Reference)
Targets
JAK1 (IC50 = 10 nM); JAK2 (IC50= 28 nM); Tyk2 (IC50= 116 nM); JAK3 (IC50= 810 nM)
ln Vitro
Th2 cell differentiation mediated by IL-4, a cytokine that signals through JAK1 and JAK3, is dose-dependently inhibited by filgotinib (GLPG0634). Moreover, filgotinib also inhibits Th1 differentiation at 1 μM or less in potency [1]. JAK2 homodimer-mediated signaling generated by PRL or EPO (IC50 > 10 μM) is not inhibited by filgotinib (GLPG0634) [2].
ln Vivo
In a rat CIA model that has been modified, filgotinib (GLPG0634; 3, 10, 30 mg/kg, po) dose-dependently inhibits the course of the disease. Filgotinib (50 mg/kg, op) inhibits the deterioration of bone and cartilage, effectively decreases the infiltration of T cells (CD3+ cells) and macrophages (F4/80+ cells) in the paw, and lowers blood levels of cytokines and chemokines, such as IL-6, IP-10, XCL1, and MCP-1[1]. In a rat model of CIA, filgotinib (GLPG0634; 0.1 and 0.3 mg/kg) demonstrated effectiveness [2].
Enzyme Assay
Biochemical assays[1]
IC50 determination.[1]
Recombinant JAK1, TYK2, JAK2, and JAK3 were used to develop activity assays in 50 mM HEPES (pH 7.5), 1 mM EGTA, 10 mM MgCl2, 2 mM DTT, and 0.01% Tween 20. The amount of JAK protein was determined per aliquot, maintaining initial velocity and linearity over time. The ATP concentration was equivalent to 4× the experimental Km value and the substrate concentration (ULight-conjugated JAK-1(Tyr1023) peptide) corresponded to the experimentally determined Km value. After 90 min incubation at room temperature (RT), the amount of phosphorylated substrate was measured by addition of 2 nM europium-anti-phosphotyrosine Ab (PerkinElmer) and 10 mM EDTA in Lance detection buffer. Compound IC50 values were determined by preincubating the enzyme with compound at RT for 60 min, prior to the addition of ATP.
Kd determination.[1]
Dissociation constants were determined at a CRO company. Proprietary fluorescently labeled ATP mimetics with fast dissociation rates (PRO13, PRO14, and PRO13 for JAK1, JAK2, and JAK3, respectively) were incubated with JH1 domains of purified JAKs in 20 mM MOPS (pH 7.5), 1 mM DTT, 0.01% Tween 20, and 500 mM hydroxyectoine (JAK3 only) for 30 min. Compounds (concentrations ranging from 520 pM to 1.1 μM) were added in 100% DMSO and time dependency of reporter displacement was measured. IC50 values corresponding to 50% probe displacement were obtained and Kd values were calculated according to the Cheng–Prusoff equation.
Cell Assay
Cellular assays[1]
STAT6 phosphorylation induced by IL-4.[1]
THP-1 cells (ATCC TIB-202) were preincubated with compound at RT for 1 h, incubated with IL-4 (10 ng/ml) at RT for 60 min, and processed for flow cytometry. Cells were fixed in Cytofix/Cytoperm buffer and permeabilized in Phosflow perm buffer III on ice for 30 min. After blocking (Fc blocking reagent), pSTAT6 was detected with mouse anti-human PE-labeled anti-pSTAT6 Ab.
STAT5 phosphorylation induced by IL-2, IL-3, and erythropoietin.[1]
NK-92 cells (ATCC CRL-2407) were IL-2 starved overnight, preincubated with compound at 37°C for 1 h, stimulated with IL-2 (1 ng/ml) at RT for 20 min, and processed for AlphaScreen analysis. TF1 cells were starved overnight in RPMI 1640 with 0.1% FBS, preincubated with compound at RT for 1 h, stimulated with IL-3 (30 ng/ml) at RT for 20 min, and processed for AlphaScreen analysis. UT-7-erythropoietin (EPO) cells (EPO-dependent derivative of UT-7; Centocor) were preincubated with compound at RT for 1 h, stimulated with EPO (1 U/ml) for 20 min, and processed for AlphaScreen analysis. pSTAT5 was measured using AlphaScreen technology essentially according to the manufacturer’s protocol.
STAT1 phosphorylation induced by IFN-α and IFN-γ.[1]
STAT1 U2OS cells (Invitrogen, catalog no. K1469) were preincubated with compound at 37°C for 1 h, treated with 30,000 U/ml IFN-αB2 (PBL IFN source, catalog no. 11115-1) or 20 ng/ml IFN-γ at 37°C for 1 h, lysed (lysis buffer containing 2 nM Tb-Ab) according to manufacturer’s protocol, and incubated at RT for 60 min. pSTAT1 was detected by time-resolved fluorescence resonance energy transfer.
STAT5 phosphorylation induced by prolactin.[1]
22Rv1 cells (ATCC CW22Rv) were starved overnight, preincubated with compound, triggered with prolactin (PRL; 500 ng/ml human PRL for 20 min), lysed in 10 mM Tris-HCl (pH 7.5), 5 mM EDTA, 150 mM NaCl, 0.5% Triton X-100, 50 mM NaF, 30 mM sodium pyrophosphate, 10% glycerol buffer containing phosphatase/protease inhibitor cocktails, and centrifuged. Cell lysate (180 μg) was used for STAT5 immunoprecipitation (anti-STAT5 polyclonal Abs, C-17; protein A-Sepharose beads). Total and phosphorylated STAT5 were measured by densitometric analysis after Western blotting.
IL-3/JAK2–induced proliferation of Ba/F3 cells.[1]
Ba/F3 cells (provided by V. Lacronique, Paris, France), which are dependent on IL-3 and JAK2 signaling, were incubated with compound at 37°C for 40 h, after which cell proliferation was analyzed by measuring ATP content.
Oncostatin M-induced STAT1 reporter assay in HeLa cells[1]
. HeLa cells (ATCC CCL-2) were transfected with a pSTAT1 reporter construct (Panomics, catalog no. LR0127). After transfection for 24 h, cells were incubated for 1 h with compound and triggered with oncostatin M (OSM; 33 ng/ml). After 20 h incubation, the cells were lysed and luciferase activity was determined with the luciferase SteadyLite kit according to the supplier’s recommendations. In parallel, β-galactosidase activity was measured in the presence of 4 mg/ml 2-nitrophenyl β-d-galactopyranoside.
Knockdown experiments.[1]
HeLa and HCT116 cells obtained from the American Type Culture Collection were transfected with 50 nM ON-TARGETplus SMARTpool small interfering RNA (siRNA) for human JAK1, JAK2, JAK3, or TYK2, or with nontargeting or GAPDHnegative control siRNAs using Lipofectamine RNAiMAX transfection reagent from Invitrogen. Four days after transfection cells were starved overnight and stimulated with IL-6/sIL-6R (both 250 ng/ml) for 20 min and pSTAT1 levels were determined using AlphaScreen technology according to the manufacturer’s protocol.
T cell differentiation studies.[1]
PBMCs were isolated from buffy coats of healthy donors using density gradient centrifugation on Lymphoprep. Naive CD4+ T cells were further isolated by depletion of non–T helper and memory CD4+ T cells using a naive CD4+ T cell isolation kit II. Isolated naive CD4+ T cells were stimulated with plate-bound anti-CD3 (3 μg/ml) and anti-CD28 (5 μg/ml) Abs in the presence of cytokines that drive differentiation into Th1, Th2, or Th17 Th subsets. For Th1 cell polarization, cells were cultured in the presence of 10 μg/ml anti–IL-4 Ab, 10 ng/ml IL-2, and 10 ng/ml IL-12. For Th2 cell polarization, cells were cultured in the presence of 10 μg/ml anti–IFN-γ Ab (Becton Dickinson), 25 ng/ml IL-4, and 10 ng/ml IL-2. For Th17 cell polarization, a mix of the following cytokines was used: 10 ng/ml IL-6, 10 ng/ml IL-1β, 1 ng/ml TGF-β, and 100 ng/ml IL-23. To monitor effects of compounds on T cell differentiation, compounds were added at indicated concentrations at the start of T cell differentiation. After 5 d, RNA was extracted using an RNeasy Mini kit, reverse transcribed, and the extent of Th subset differentiation was monitored by determining expression of IFN-γ (Th1 marker), IL-13 (Th2 marker), or IL-17F (Th17 marker) using real-time PCR on the ViiA7 thermocycler with predesigned TaqMan Assay-on-Demand gene expression primer/probe sets. Gene expression was normalized to 18S and expressed as ΔCt values, with ΔCt = Ctgene − Ct18S or expressed as relative mRNA level of specific gene expression as obtained using the 2−ΔCt method.
Animal Protocol
Pharmacokinetics[1]
Formulations.[1]
GLPG0634 was formulated in polyethyleneglycol 200/0.9% NaCl (60/40; v/v) for i.v. administration and in 0.5% (v/v) methylcellulose for oral administration for all in vivo studies described. Compound purity was >95% as measured by HPLC. Animals.[1]
Male Sprague Dawley rats (180–200 g) and CD1 mice (23–25 g) were obtained from Janvier and Harlan, respectively. Two days before administration of compound, rats underwent surgery to place a catheter in the jugular vein under isoflurane anesthesia. Animals were deprived of food for at least 16 h before oral dosing until 4–6 h after. Before oral dosing, animals were deprived of food for at least 12 h before compound administration until 4 h after administration. All in vivo experiments were carried out in a dedicated pathogen-free facility (22°C).

Pharmacokinetic studies.[1]
GLPG0634 was orally dosed as a single esophageal gavage at 5 mg/kg (dosing volume of 5 ml/kg) and i.v. dosed as a bolus via the caudal vein at 1 mg/kg (dosing volume of 5 ml/kg). In the rat study, each group consisted of three rats and blood samples were collected via the jugular vein. In the mouse study, each group consisted of 21 mice (n = 3/time point) and blood samples were collected by intracardiac puncture under isoflurane anesthesia. Lithium heparin was used as anticoagulant and blood was taken at 0.05, 0.25, 0.5, 1, 3, 5, and 8 h (i.v. route) and 0.25, 0.5, 1, 3, 5, 8, and 24 h (by mouth).

GLPG0634 plasma concentrations were determined by liquid chromatography–tandem mass spectrometry with a lower limit of quantification of 2 ng/ml. Pharmacokinetic parameters were calculated by noncompartmental analysis using WinNonlin software.
In vivo pharmacology[1]
Rodent CIA models.[1]
Animals.[1]
Dark Agouti rats (females, 7–8 wk old) and DBA/1J mice (male, 6 wk old) were obtained from Janvier.

Materials.[1]
CFA and IFA were purchased from Difco (Detroit, MI). Bovine collagen type II (CII) was used. All other reagents used were of reagent grade and all solvents were of analytical grade.

CIA.[1]
One day before the start of the experiment, CII solution (2 mg/ml) was prepared with 0.05 M acetic acid and stored at 4°C. Just before the immunization, equal volumes of IFA and CII were mixed by a homogenizer in a precooled glass bottle in an ice water bath. For rat CIA experiments, the emulsion (0.2 ml) was injected intradermally at the base of the tail at day 1 and again at day 8. This immunization method was modified from published methods. The in vivo efficacy of GLPG0634 was determined after daily oral administration for a period of 14 d after onset of disease (average clinical score at onset, 2.5 ± 0.3; 10 rats/treatment group) over the dose range 0.1–30 mg/kg. The TNF-α blocker etanercept was administered three times per week at 10 mg/kg by i.p. injection. A fully active dose was reported to require repeated dosing in the 3–9 mg/kg range. In our model of Dark Agouti female rats, disease normalization was reached for 10 mg/kg etanercept dosed three times a week i.p. as measured by clinical score, inflammation, bone resorption, pannus, and cartilage damage. At day 7 or 11, 200 μl blood was collected by retro-orbital puncture with lithium heparin as anticoagulant at predose and 1, 3, and 6 h (n = 2 or 3/time point) for steady-state pharmacokinetics analysis. At sacrifice, hind paws were removed for x-ray analysis and histological examination. A Tukey multiple comparison test was used to perform a meta-analysis of three studies carried out for GLPG0634. The score of each rat was divided by the average score obtained for vehicle in the same readout and study and multiplied by 100. Relative scores were averaged per readout for all animals present in all studies that received the same dose. For mouse CIA experiments, the IFA/CII emulsion (0.2 ml) was injected intradermally at the base of the tail at day 1 and again at day 21. This immunization method was modified from published methods. The in vivo efficacy of GLPG0634 was determined after daily oral administration for a period of 14 d after onset of disease (average clinical score at onset, 2.4 ± 0.6; 10 mice/treatment group) over the dose range 50 mg/kg twice daily. Administration of etanercept and pharmacodynamic and pharmacokinetic analyses were essentially carried out as described for the rat CIA model.
30 mg/kg daily in Rats); 50 mg/kg twice daily in Mice
In the rat model of collagen-induced arthritis (CIA), oral administration of GLPG0634 shows a marked protection from bone damage at dose of 3 mg/kg. It reduces the infiltration of inflammatory cells significantly from 1 mg/kg onward
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Filgotinib is rapidly absorbed after oral administration. Median peak plasma concentrations occurred 2-3 hours post-dose for filgotinib and 5 hours post-dose for GS-829845. Steady-state concentrations can be observed in 2-3 days for filgotinib and in 4 days for GS-829845. Food does not appear to have a significant effect on the absorption of filgotinib; therefore, the medication can be administered without regard to food. After repeated oral dosing of filgotinib 200 mg, the reported Cmax and AUCτ values of filgotinib were 2.15 ug/mL and 6.77 ugxh/mL, respectively. For GS-829845 (the major metabolite) the reported Cmax was 4.43 ug/mL and the reported AUCτ was 83.2 ugxh/mL.
Of the total administered dose of filgotinib, approximately 87% undergoes renal elimination while 15% undergoes faecal elimination.
Metabolism / Metabolites
Carboxylesterase enzymes are involved in the metabolism of filgotinib. The carboxylesterase 2 (CES2) isoform is chiefly responsible for metabolizing filgotinib to its major metabolite, GS-829845. Although carboxylesterase 1 (CES1) plays a less prominent role in the biotransformation of filgotinib, in vitro studies have demonstrated that CES1 will partially compensate in the event of CES2 saturation. GS-829845 is thus far the only major circulating metabolite to have been identified.
Biological Half-Life
The half-life of filgotinib is estimated to be 7 hours, while the half-life of its active metabolite GS-829845 is estimated to be 19 hours.
Toxicity/Toxicokinetics
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Filgotinib is not approved in the United States by the Food and Drug Administration. No information is available on the clinical use of filgotinib during breastfeeding. The European manufacturer recommends that breastfeeding be discontinued during filgotinib therapy.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Approximately 55-59% of filgotinib is protein-bound, while 39-44% of the active metabolite GS-829845 is protein-bound.
References

[1]. Preclinical characterization of GLPG0634, a selective inhibitor of JAK1, for the treatment of inflammatory diseases. J Immunol. 2013, 191(7), 3568-3577.

[2]. Triazolopyridines as Selective JAK1 Inhibitors: From Hit Identification to GLPG0634. J Med Chem. 2014 Nov 17.

Additional Infomation
Pharmacodynamics
In addition to targeted Janus kinase (JAK) 1 inhibition, filgotinib targets pro-inflammatory cytokine signalling by inhibiting IL-6 induced STAT1 phosphorylation. Serum C-reactive protein levels are also reduced in response to filgotinib administration.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C21H23N5O3S
Molecular Weight
425.50
Exact Mass
425.152
Elemental Analysis
C, 59.28; H, 5.45; N, 16.46; O, 11.28; S, 7.54
CAS #
1206161-97-8
Related CAS #
GLPG0634 analog;1206101-20-3;Filgotinib maleate;1802998-75-9;Filgotinib-d4;2041095-50-3; 1206161-97-8; 1540859-07-1 (HCl hydrate)
PubChem CID
49831257
Appearance
Off-white to gray solid powder
Density
1.5±0.1 g/cm3
Index of Refraction
1.748
LogP
0.79
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
6
Rotatable Bond Count
5
Heavy Atom Count
30
Complexity
715
Defined Atom Stereocenter Count
0
InChi Key
RIJLVEAXPNLDTC-UHFFFAOYSA-N
InChi Code
InChI=1S/C21H23N5O3S/c27-20(17-8-9-17)23-21-22-19-3-1-2-18(26(19)24-21)16-6-4-15(5-7-16)14-25-10-12-30(28,29)13-11-25/h1-7,17H,8-14H2,(H,23,24,27)
Chemical Name
N-(5-(4-((1,1-dioxidothiomorpholino)methyl)phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl)cyclopropanecarboxamide.
Synonyms
GLPG-0634; PubChemSID 163643231; GLPG0634; 1206101-20-3; Filgotinib; GLPG0634; 1206161-97-8; N-(5-(4-((1,1-dioxidothiomorpholino)methyl)phenyl)-[1,2,4]triazolo[1,5-a]pyridin-2-yl)cyclopropanecarboxamide; Filgotinib (GLPG0634); N-[5-[4-[(1,1-dioxo-1,4-thiazinan-4-yl)methyl]phenyl]-[1,2,4]triazolo[1,5-a]pyridin-2-yl]cyclopropanecarboxamide; GLPG 0634; Filgotinib
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 85 mg/mL (199.8 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.88 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (5.88 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (5.88 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


Solubility in Formulation 4: ≥ 2.5 mg/mL (5.88 mM) (saturation unknown) in 5% DMSO + 40% PEG300 + 5% Tween80 + 50% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 5: ≥ 2.5 mg/mL (5.88 mM) (saturation unknown) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

Solubility in Formulation 6: 4% DMSO+30% PEG 300+ddH2O: 3mg/mL

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.3502 mL 11.7509 mL 23.5018 mL
5 mM 0.4700 mL 2.3502 mL 4.7004 mL
10 mM 0.2350 mL 1.1751 mL 2.3502 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT05817942 Recruiting Drug: Filgotinib Ulcerative Colitis Galapagos NV June 12, 2023
NCT05323591 Recruiting Drug: Filgotinib Rheumatoid Arthritis Galapagos NV May 3, 2022
NCT04871919 Recruiting Drug: Filgotinib Rheumatoid Arthritis Galapagos NV May 11, 2021
NCT05785611 Recruiting Drug: Filgotinib
Drug: Placebo
Axial Spondyloarthritis Galapagos NV April 5, 2023 Phase 3
Biological Data
  • Filgotinib (GLPG0634)

    GLPG0634 inhibits the differentiation of Th1, Th2, and Th17 cells.J Immunol.2013 Oct 1;191(7):3568-77.

  • Filgotinib (GLPG0634)

    GLPG0634 dose-dependently prevents disease progression in the therapeutic rat CIA model.J Immunol.2013 Oct 1;191(7):3568-77.

  • Filgotinib (GLPG0634)

    GLPG0634 is efficacious in a mouse therapeutic CIA model.J Immunol.2013 Oct 1;191(7):3568-77.

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