A Multicentre, Randomised, Double-blind, Placebo-controlled Study to Evaluate the Efficacy and Safety of GSK2982772 in Participants With Moderate to Severe Plaque Psoriasis

Plaque psoriasis is a chronic relapsing inflammatory skin disease that is characterized by keratinocyte hyper-proliferation and epidermal hyperplasia. Standard treatment for psoriasis generally requires long-term use of topical therapies, psoralen and ultraviolet A (PUVA), ultraviolet B (UVB) and/or systemic immunosuppressant therapies to achieve and maintain adequate disease control. This is a multicenter, randomized, double-blind study conducted in participants with moderate to severe plaque psoriasis. The study will evaluate the efficacy, safety, pharmacokinetic and pharmacodynamics profile of 960 milligram (mg) GSK2982772 administered as a once daily modified release (MR) formulation. Participants will be randomized in a 2:1 ratio to receive either 960 mg GSK2982772 or placebo for 12 weeks. The duration of the study, including Screening and follow-up, will be approximately 21 weeks for each participant.

Start Date28 Sep 2020

Sponsor / Collaborator

GSK Plc

NCT03649412

/ CompletedPhase 1

A Two Part, Non-randomised, Open Label Study Designed to Assess the Pharmacokinetic Profile of Modified Release Prototype Coated Tablet Formulations of GSK2982772 Relative to an Immediate Release Reference Tablet Formulation at a Fixed Strength (Part A) and the Pharmacokinetic Profile of Alternative Tablet Strengths of the Selected Modified Release Prototype Coated Tablet Formulation (Part B, Optional) in Healthy Participants

Previous clinical studies of immediate release (IR) formulations of GSK2982772 resulted in a high peak to trough ratio of GSK2982772. Additionally, the short half-life for GSK2982772 (approximately 2 to 3 hours) necessitates twice a daily (BID) or thrice daily (TID) dosing of an IR formulation. As a result, MR formulations using a polymer matrix approach with minitablets in capsule and MR tablet formulations were investigated. The emerging PK data of the MR formulations investigated to date have demonstrated that a once daily (QD) PK profile can be achieved in the fasted state but the polymer matrix formulation is susceptible to food effects when administered with a high fat breakfast. The purpose of this study is to evaluate MR prototype coated tablet formulations. This study will evaluate the PK of MR prototype coated tablet formulations of GSK2982772. The study is divided into two parts; Part A and Part B. The MR tablet coating used in Part A and the initial periods of Part B will have an aperture drilled into the enteric coating of either side of the tablet. This allows some drug release to commence in the stomach whilst providing controlled release throughout the gastrointestinal (GI) tract. In Part B only, a new investigational medicinal product (IMP) will be manufactured to allow comparison of the tablet coating either with apertures (i.e., drilled) or without apertures (i.e., full coat/non drilled). Part A will be a 6-period, 6-way fixed sequence design, up to 4 MR tablet prototype coated formulations will be evaluated in fasted state at 240 milligrams (mg). Periods 1, 2 and 3 will evaluate MR1, IR tablet and MR2 respectively. Periods 4, 5 and 6 will be flexible and the dosing regimen will be dependent on the outcome of Periods 1 to 3. In addition, the impact of food (high fat meal, standard breakfast or administration 30 or 60 minutes before a standard breakfast) on selected MR prototype coated tablet formulations may also be evaluated in Period 4, 5 or 6 of Part A. Each inpatient period for MR regimens (Periods 1, 3, 4 to 6) will consist of 4 days and 3 nights, and the inpatient period for the IR tablet (Period 2) will consist of 3 days and 2 nights. There will be a minimum washout of 7 days between doses, and a follow-up visit will occur at 7 to 9 days after the last study treatment. The Part B of the study will be a 7-period fixed sequence which will evaluate the selected MR prototype coated tablet formulation(s) at different tablet strengths or as multiple unit doses and with or without apertures in the tablet coatings. There will be an interim review after each period 1 to 5 of Part B to select the dose level, formulation and prandial status for each subsequent period. An interim data review after Part B Period 6 will determine if optional Period 7 is required and the dose level, dosing time (morning or evening), formulation and prandial status for that period. Each inpatient period will consist of a 4-day and 3-night with a minimum of 7 days washout between doses. A follow-up visit will occur at 7 to 9 days after the last study treatment. Approximately 33 subjects will be enrolled in the study. The total duration for Part A will be approximately 10-12 weeks and 10-14 weeks for Part B (including screening period of approximately 4 weeks).

Start Date26 Sep 2018

Sponsor / Collaborator

GSK Plc

[+1]

NCT03590613

/ CompletedPhase 1

A Single-centre, Randomized, Double-blind, Dose-ascending, Placebo-controlled Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of Oral TID Doses (One Day) of GSK2982772 in Japanese Healthy Male Subjects

The study plans to enroll approximately 12 subjects. The main objective of the study is to assess the safety, tolerability and pharmacokinetics (PK) of the three times a day (TID), dosing of GSK2982772, in Japanese healthy male subjects. The study will comprise of four study periods each at least 7 days in duration with subjects in-house for 4 nights (through 72 hrs after the first dose). During each treatment period (TP), subjects will be admitted to the unit the day before dosing and will be discharged after completion of the 72 hours post-dose assessments. There will be a washout of atleast 7-days between the TP doses for each individual, post which there will be 7-days follow-up. The dose range proposed in this study is based on a low starting dose, which will be escalated to the highest dose that is intended for the Phase 2b dose range study. The decision to proceed to the next dose-level, of GSK2982772 within the study will be made by principal investigator and GSK Medical Monitor per each dosing periods. The study duration is approximately 22 weeks.

Start Date19 Jul 2018

Sponsor / Collaborator

GSK Plc

100 Clinical Results associated with GSK-2982772

100 Translational Medicine associated with GSK-2982772

100 Patents (Medical) associated with GSK-2982772

Literatures (Medical) associated with GSK-2982772

01 Aug 2025·BIOMEDICINE & PHARMACOTHERAPY

Cilostazol attenuates vascular inflammation via the regulation of TICAM1/IRF3 signaling pathway

Article

Author: Chiu, Hui-Wen ; Shih, Chun-Che ; Sung, Li-Chin ; Huang, Tzu-Hsuan ; Huang, Hung-Jin

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality and morbidity worldwide. Chronic inflammation of the endothelium is a pivotal process in the pathogenesis of ASCVD. Therefore, the identification of pro-atherogenic gene expression and subsequent screening out of potential therapeutic agents for vascular inflammation is an attractive issue. The TICAM1 and IRF3 genes were identified as susceptibility genes whose expression was upregulated in lipopolysaccharide (LPS)-induced vascular inflammation. Cilostazol was found to be the most potential bioactive drug for the TICAM1 proteins. Cilostazol pretreatment also increased autophagy and decreased necroptosis and NLRP3/NLRP6 inflammasome formation, as well as the pro-inflammatory cytokine interleukin-1β, in vitro and in vivo. Additionally, cilostazol significantly attenuated the TNF-α-induced elevation in circulating adhesion molecules. Furthermore, cilostazol treatment markedly reduced aortic wall thickening in TNF-α-challenged mice. After experiments into mechanistic understanding, we found that the candidate drug cilostazol reduces vascular inflammation and possibly atherosclerosis progression. Therefore, this study can offer broader evidence of cilostazol for treating individuals with ASCVD or at high risk of ASCVD. Further prospective clinical trials are warranted to confirm its application and effectiveness.

01 Jan 2025·ARCHIV DER PHARMAZIE

Design and synthesis of pyridazin‐4‐one derivatives as necroptosis inhibitors

Article

Author: Geng, Meiyu ; Zhang, Hefeng ; Liu, Kaiyuan ; Ai, Jing ; Duan, Wenhu ; Feng, Dazhi ; Zhou, Xuan ; Fang, Chen ; Peng, Xia ; An, Yuxiang ; Wang, Tianchen

Abstract:

Necroptosis is a regulated inflammatory cell death process that is closely associated with autoimmune diseases, acute ischemic injuries, neurodegenerative disorders, and so on. Due to the crucial role of receptor‐interacting protein kinase 1 (RIPK1) in the necroptosis pathway, RIPK1 inhibitors are believed to have great potential in the treatment of necroptosis‐related diseases. In this article, we reported a series of pyridazin‐4‐one derivatives as potent necroptosis inhibitors for both human and mouse cells. The representative compound 13 exhibited favorable RIPK1 selectivity and dose‐dependently inhibited RIPK1 phosphorylation. The in vivo pharmacokinetic study indicated that compound 13 was an orally available candidate. Finally, molecular docking and molecular dynamics simulations were performed to elucidate the binding pattern of compound 13 with RIPK1. Collectively, compound 13 represents a promising lead compound for the future development of RIPK1‐targeted necroptosis inhibitors.

12 Dec 2024·JOURNAL OF MEDICINAL CHEMISTRY

Polypharmacological Drug Design Guided by Integrating Phenotypic and Restricted Fragment Docking Strategies

Article

Author: Wang, Xiaobing ; Wan, Siyuan ; Ma, Liangliang ; Li, Xinxin ; Luo, Zhongwen ; Kong, Lingyi ; Zhou, Han ; Chen, Yifan ; Yin, Fucheng ; Zhang, Yonglei ; Li, Shang

Polypharmacological drugs are of great value for treating complex human diseases by the combinative modulation of several biological targets. However, multitarget drug design with more than two targets is challenging and generally discovered by serendipity. Herein, a restricted fragment docking (RFD) computational method combined with a phenotypic discovery approach was developed for rational polypharmacological drug design. Via genetic and drug combination studies in a microglial phenotype, we first identified novel synergistic effects by triple target modulation toward RIPK1, MAP4K4, and ALK. Drawing on the RFD method to explore virtual chemical spaces in three target pockets, we identified a lead compound, LP-10d, that precisely modulated RIPK1/MAP4K4/ALK for synergistic microglial protection with low nanomolar potency. LP-10d showed polypharmacology against multiple neuropathologies in the 3xTg Alzheimer's disease mouse model. Our study revealed a potential application of the RFD method, which is valuable to further polypharmacological drug discovery involved in clinical studies for treating complex human diseases.

News (Medical) associated with GSK-2982772

20 Mar 2026

·allsci.com

Genentech terminates study of flizasertib for cardiac surgery-associated acute kidney injury

Genentech, Inc., a wholly owned subsidiary of Hoffmann-La Roche, has terminated a Phase II study evaluating the selective RIPK1 inhibitor GDC-8264 for the prevention of acute kidney injury in patients undergoing cardiac surgery. According to the ClinicalTrials.gov registry update, Genentech indicated the study was “unlikely to demonstrate a statistically significant clinical benefit” as the basis for the early stop. The trial, which had enrolled 67 participants across sites in the United States, Europe, Australia, New Zealand, South Korea, and Canada, was designed to test whether perioperative RIPK1 inhibition could reduce kidney complications following cardiopulmonary bypass procedures. The termination raises fresh questions about the future of clinical development for GDC-8264 — also known as flizasertib or RO7288817 — although Roche has not publicly confirmed whether the program has been fully discontinued. The Phase II study was a randomized, double-blind, placebo-controlled trial conducted in two sequential parts. Genentech designed the study to enroll adults aged 40 and older who were scheduled for non-emergent cardiac surgery requiring cardiopulmonary bypass — including isolated coronary artery bypass grafting, surgical aortic or mitral valve replacement or repair, and combined procedures. Eligible participants had to carry at least one or two predefined risk factors for acute kidney injury, depending on the type of surgery. The trial’s primary endpoint was the percentage of participants who developed major adverse kidney events within 90 days of surgery, a composite measure known as MAKE90. The scientific hypothesis underpinning the trial was that RIPK1-mediated necroptosis — a pro-inflammatory form of regulated cell death — plays a central role in renal ischemia-reperfusion injury during cardiac surgery. Preclinical studies, including work by Linkermann et al. (Kidney International, 2012), had demonstrated that RIPK1 inhibition reduced tubular cell necroptosis and preserved renal function in murine models of kidney injury. GDC-8264 had shown potent on-target pharmacodynamic activity in a Phase I healthy volunteer study, where it rapidly and completely inhibited release of CCL4, a downstream chemokine marker of RIPK1 pathway activation. The gap between preclinical promise and clinical outcome is not unusual in this therapeutic area. Cardiac surgery-associated acute kidney injury affects up to 30% of surgical patients and is linked to increased mortality, prolonged hospitalization, and progression to chronic kidney disease. Yet no pharmacological intervention has been approved to prevent it. The pathophysiology involves multiple overlapping mechanisms — hemodynamic instability, inflammation, oxidative stress, nephrotoxin exposure — making it difficult to achieve clinically meaningful benefit by targeting a single pathway. The GDC-8264 setback extends a broader pattern of clinical disappointments for the RIPK1 inhibitor class. Beyond Genentech, other sponsors to encounter difficulties include GlaxoSmithKline with GSK2982772, the first RIPK1 inhibitor to enter clinical research in 2014, which was eventually returned to the research stage and is no longer listed in the company’s active pipeline. Sanofi scrapped its last remaining Denali Therapeutics-partnered RIPK1 inhibitor in January 2026. Eli Lilly pulled out of central nervous system (CNS)-focused development of RIPK1 inhibitors partnered with Rigel Pharmaceuticals in November 2025, but continues to develop ocadusertib (LY3871801/R552) for rheumatoid arthritis (Phase II stage) under that partnership. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

Phase 2Phase 1Clinical Result

19 Mar 2026

·www.fiercebiotech.com

Genentech shreds RIPK1 inhibitor from pipeline after early ph. 2 failure

The Roche subsidiary was testing flizasertib’s ability to treat acute kidney injury after heart surgery, a common complication that can follow procedures like coronary artery bypass, valve replacements and aortic surgeries.\n Genentech has elected to stop a phase 2 trial of a RIPK1 inhibitor early and dump the asset after an analysis revealed the candidate was unlikely to meet the study’s primary endpoint.Flizasertib, also known as GDC-8264, was removed from Genentech’s pipeline in the first quarter of this year, a company spokesperson confirmed to Fierce Biotech, after interim data “indicated that the study was unlikely to demonstrate a significant clinical benefit.”The Roche subsidiary was testing flizasertib’s ability to treat acute kidney injury after heart surgery, a common complication that can follow procedures like coronary artery bypass, valve replacements and aortic surgeries due to reduced blood flow to the filtering organs.The terminated study was a randomized, placebo-controlled phase 2 trial that began in January 2025 and enrolled 67 patients, according to the federal clinical trials database. The primary efficacy endpoint, which flizasertib was not set to deliver on, was the percentage of patients who develop persistent complications in the 90 days following a surgery-induced kidney injury.Genentech announced the discovery of GDC-8264 last fall in a paper (PDF) published in the Journal of Medicinal Chemistry. At the time, the biotech’s scientists described the small molecule as having “excellent target selectivity and druglike attributes for once-daily oral dosing.”Flizasertib’s descent is another blow for the RIPK1 inhibitor field, which has struggled to produce an approved medicine despite numerous biotechs and Big Pharmas pursuing the target. RIPK stands for receptor-interacting serine/threonine-protein kinase, with RIPK1 part of a family of enzymes that help regulate inflammation and cell death. GSK had the first-ever RIPK1 inhibitor okayed for clinical research back in 2014, but later kicked it back to the research stage; that asset, GSK2982772, is no longer listed in GSK’s pipeline. The British pharma also dropped a different candidate in the class for the development of prostate cancer in 2019. French drugmaker Sanofi bought into the modality in 2018 through a pact with Denali Therapeutics, but has steadily pulled back due to a string of phase 2 failures. Sanofi scrapped its last remaining Denali RIPK1 inhibitor at the end of January.Eli Lilly, too, has had a rethink of RIPK1. After signing a deal worth as much as $960 million with Rigel Pharmaceuticals back in 2021, Lilly reneged on the central nervous system-focused portion of the partnership. The star of that deal, though, Rigel’s ocadusertib (now coded LY3871801), is still being tested in a phase 2 trial for rheumatoid arthritis.Meanwhile, there may be potential for an already approved drug to be repurposed as a RIPK1 inhibitor. Last summer, a team of Korean scientists discovered that phensuximide, which was once used to treat epilepsy, can restrain RIPK1’s inflammatory activity.

Phase 2Clinical Trial FailureLicense out/in

30 Nov 2022

·www.biospace.com

Nimble Therapeutics names Pete Gough as Chief Scientific Officer

MADISON, Wis.--(BUSINESS WIRE)-- Nimble Therapeutics, an industry-leading peptide therapeutics company, today announced the appointment of Pete Gough, D. Phil. as Chief Scientific Officer (CSO). In this newly created role, Dr. Gough will spearhead the expansion of Nimble’s internal drug discovery capabilities that will enable further development of its own pipeline of proprietary therapeutics and drive Nimble towards becoming a fully integrated biotechnology company. Dr. Gough has more than 25 years of experience in discovery research, both in academic settings as well as in the life sciences industry, and a track record of success in drug discovery and development, driving research programs into clinical study by building and leading high-performance teams. Prior to joining Nimble, Pete served as the CSO for Inzen Therapeutics, a Flagship company pioneering the newly discovered science of Thanokine Biology. At Inzen, he helped advance the company from seed stage to a successful Series B through the development of their pipeline of potentially transformational Immuno-Oncology therapeutics. Previously, Pete spent 15 years at GSK in roles of increasing responsibility. He served as Head of the Hepatitis B Virus Discovery Performance Unit (DPU) where he led GSK’s efforts to develop a functional cure for HBV including proof of concept studies for bepirovirsen. He also served as Head of the Host Defense DPU, and prior to that was Head of Biology and DMPK in the Pattern Recognition Receptor DPU. Pete led, and oversaw, the discovery and development of a number of clinical assets across multiple therapeutic areas including RIP1 kinase inhibitor GSK2982772 and STING agonist GSK3745417. “We’re excited to welcome Pete to our management team at Nimble,” said Jigar Patel, PhD, Founder and CEO of Nimble Therapeutics. “Since our formation in 2019, Nimble has worked diligently to optimize and validate our peptide discovery platform. Pete brings invaluable experience in drug discovery and development across multiple therapeutic areas that will enable Nimble to deliver on the promise of peptide therapeutics through progressing and expanding our own internal pipeline.” “Nimble has built the industry leading platform for discovering peptide therapeutics that solves for the challenges that everyone else in the field is struggling with,” said Dr. Gough. “I’m very excited to be part of the team and to help realize the truly transformative nature of the Nimble platform by advancing novel medicines into the clinic.” Earlier in his career, Pete was a Research Assistant Professor in the Department of Pathology at the University of Washington. He received his D. Phil. and M. A. from the University of Oxford. Pete has authored/co-authored over 100 scientific papers in peer-reviewed journals and has been an invited speaker at numerous academic institutions and scientific conferences. About Nimble Therapeutics Nimble is a biotechnology company dedicated to delivering on the promise of peptide therapeutics. Leveraging a paradigm-shifting peptide drug discovery and development engine, Nimble combines massively parallel solid-phase synthesis, unrivaled chemical and structural diversity, sophisticated assays, and powerful analytics to efficiently and intelligently discover and develop next generation peptide therapeutics. Nimble has extensively validated its platform to identify highly biologically active compounds for multiple programs, spanning a wide variety of therapeutic target classes. Connect with us on LinkedIn at or visit our website at to learn more.

Executive Change

100 Deals associated with GSK-2982772

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Indication	Highest Phase	Country/Location	Organization	Date
Psoriasis	Phase 2	Poland	GSK Plc	28 Sep 2020
Colitis, Ulcerative	Phase 2	United States	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	Germany	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	Netherlands	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	Poland	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	Russia	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	Sweden	GSK Plc	15 Nov 2016
Colitis, Ulcerative	Phase 2	United Kingdom	GSK Plc	15 Nov 2016
Rheumatoid Arthritis	Phase 2	Germany	GSK Plc	17 Oct 2016
Rheumatoid Arthritis	Phase 2	Italy	GSK Plc	17 Oct 2016

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04316585 (CTgov)	Phase 1	Plaque psoriasis	29	GSK2982772 (GSK2982772 960 mg)	afydaescpq = efgnsdnhyy ghuphchlum (rifelogpzw, kfdjbjnjup - ierqyfnagr) View more	-	18 Mar 2024
				placebo+GSK2982772 (Placebo)	afydaescpq = vsynhrqfty ghuphchlum (rifelogpzw, ocuqjfcxiv - iqnhjvpndy) View more
NCT02903966 (Pubmed \| BMJ Open Gastroenterol) Manual	Phase 2	Colitis, Ulcerative	36	GSK2982772	vnxeibavck(opiemrugdz) = jhvoxzyldf kvghwgbasl (iesgrpozsc )	Positive	01 Aug 2021
				Placebo	vnxeibavck(opiemrugdz) = zkhfrbawpg kvghwgbasl (iesgrpozsc )
NCT02858492 (Pubmed \| Arthritis Res Ther) Manual	Phase 2	Rheumatoid Arthritis	52	GSK2982772	glxnolcmsn(wuyiypnxfk) = bkmgkwzwmt ndhsujfdhk (pbtsiehxer ) View more	Negative	16 Mar 2021
				Placebo	glxnolcmsn(wuyiypnxfk) = agpuboflby ndhsujfdhk (pbtsiehxer ) View more
NCT02903966 (CTgov)	Phase 2	Colitis, Ulcerative	36	Placebo (Part A: Placebo TID DB)	hygfuphvgv = gfrjsvvmca xtcwdlztmz (pijgezyjza, xejqswftve - tlijsrvowz) View more	-	11 Jun 2020
				GSK2982772 (Part A: GSK2982772 60 mg TID DB)	hygfuphvgv = cjdqumwkmv xtcwdlztmz (pijgezyjza, zhaxxizcib - faeyamjgcv) View more
NCT02858492 (CTgov)	Phase 2	Rheumatoid Arthritis	52	Placebo (Placebo BID)	pocrpzhjwk = plnttfyhbv opdrfrtzih (ixcqrovkiz, dlsppkjypb - zorgdbopsu) View more	-	01 Nov 2019
				Placebo (Placebo TID)	pocrpzhjwk = spdbswtssz opdrfrtzih (ixcqrovkiz, oiewafelcd - ltzthceerb) View more
NCT03305419 (CTgov)	Phase 1	Autoimmune Diseases	62	placebo (Part A:Placebo)	xymujvqynx = stqfpxzimp keorxtixyp (bhmyydscez, fkylurkvao - ittawcswwb) View more	-	01 Nov 2019
				GSK2982772 (Part A:GSK2982772 120 mg TID)	xymujvqynx = xmnzhzhufl keorxtixyp (bhmyydscez, arwyfmyayg - bshohwqwtc) View more
NCT03590613 (CTgov)	Phase 1	Autoimmune Diseases	13	PBO+GSK2982772 (Placebo)	vdbrufjeke = sdphmolrob lrublttfvz (nemfpvlmyr, xjmhrpwdbq - ybrryhamdt) View more	-	17 Sep 2019
				GSK2982772 (GSK2982772 60 mg)	vdbrufjeke = lvxjgfofzq lrublttfvz (nemfpvlmyr, tgfbifijwz - lifrrtqfcj) View more
NCT02776033 (CTgov)	Phase 2	Plaque psoriasis	65	placebo (Placebo)	fimtuytdtf = kmdmqjetqy cjbkwkoqjm (bxxgxrlxgk, ndhflhlbdw - rptsxwjblw) View more	-	22 Aug 2019
				GSK2982772 (GSK2982772 60 mg BID)	fimtuytdtf = jmygtgwslr cjbkwkoqjm (bxxgxrlxgk, pabpgbmalj - btlnxtscfy) View more
NCT02302404 (Pubmed) Manual	Phase 1	-	-	GSK2982772	lxwrqzmcjb(yldorucxuu) = there were no serious AEs. oimfudutym (ersgghfmop ) View more	Positive	01 Dec 2017
				Placebo

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