An Open Label Study on the Effects of a Short Course of SB480848 (Darapladib) on Contents of Cantharidin-Induced Inflammatory Blisters in Subjects With Type 2 Diabetes Mellitus

This will be an exploratory, open-label, single sequence, two part study (Part A and an optional Part B). The aim of this study will be to assess whether systemic inhibition of Lipoprotein associated phospholipase A2 (Lp-PLA2) in humans, effected by 11 days of once daily dosing to steady state with 160 milligrams (mg) of enteric coated (EC) darapladib, will specifically reduce the number of macrophages and/or result in a higher proportion of M2 macrophages in skin blisters induced by cantharidin (a chemical agent that causes blisters). In Part A of the study, a cohort of 8 subjects with type 2 diabetes mellitus will be recruited. In Part B of the study, a cohort of 8 additional healthy subjects with matching age (+/- 24 months) and gender to Part A may be recruited.

Start Date26 Feb 2014

Sponsor / Collaborator

GSK Plc

NCT02000804

/ CompletedPhase 1

A Study to Evaluate the Pharmacokinetics, Pharmacodynamics and Safety of 160 mg Enteric-coated Micronised Free Base Darapladib in Healthy Chinese Subjects.

This study is to evaluate pharmacokinetics (PK), pharmacodynamics (PD) and safety of 160 mg enteric-coated micronised free base darapladib in healthy Chinese subjects.

Start Date23 Oct 2013

Sponsor / Collaborator

GSK Plc

NCT01873339

/ CompletedPhase 1

An Open-label, Single-sequence Study to Evaluate the Potential CYP 3A4 Pharmacokinetic Interaction of Darapladib (SB-480848) in Healthy Subjects

This study will determine the effect of single and repeat administration of darapladib, a novel, selective, orally active inhibitor of lipoprotein associated phospholipase A2 (Lp-PLA2) currently under clinical development on the pharmacokinetics of a single oral dose of midazolam, a cytochrome P450 3A4 (CYP3A4) probe substrate. This study will investigate the inductive and inhibitory effect of darapladib on CYP3A4 metabolic pathway.

Start Date19 Jun 2013

Sponsor / Collaborator

GSK Plc

100 Clinical Results associated with Darapladib

100 Translational Medicine associated with Darapladib

100 Patents (Medical) associated with Darapladib

199

Literatures (Medical) associated with Darapladib

01 Oct 2025·Neural Regeneration Research

Inhibiting ceramide synthase 5 expression in microglia decreases neuroinflammation after spinal cord injury

Article

Author: Liu, Bin ; Liu, Chenrui ; Fang, Xingxing ; Wu, Yingjie ; Rong, Limin ; Zhang, Liangming ; Lu, Yubao ; Zhang, Wei ; Shen, Ruoqi

JOURNAL/nrgr/04.03/01300535-202510000-00026/figure1/v/2024-11-26T163120Z/r/image-tiff Microglia, the resident monocyte of the central nervous system, play a crucial role in the response to spinal cord injury. However, the precise mechanism remains unclear. To investigate the molecular mechanisms by which microglia regulate the neuroinflammatory response to spinal cord injury, we performed single-cell RNA sequencing dataset analysis, focusing on changes in microglial subpopulations. We found that the MG1 subpopulation emerged in the acute/subacute phase of spinal cord injury and expressed genes related to cell pyroptosis, sphingomyelin metabolism, and neuroinflammation at high levels. Subsequently, we established a mouse model of contusive injury and performed intrathecal injection of siRNA and molecular inhibitors to validate the role of ceramide synthase 5 in the neuroinflammatory responses and pyroptosis after spinal cord injury. Finally, we established a PC12-BV2 cell co-culture system and found that ceramide synthase 5 and pyroptosis-associated proteins were highly expressed to induce the apoptosis of neuron cells. Inhibiting ceramide synthase 5 expression in a mouse model of spinal cord injury effectively reduced pyroptosis. Furthermore, ceramide synthase 5-induced pyroptosis was dependent on activation of the NLRP3 signaling pathway. Inhibiting ceramide synthase 5 expression in microglia in vivo reduced neuronal apoptosis and promoted recovery of neurological function. Pla2g7 formed a “bridge” between sphingolipid metabolism and ceramide synthase 5-mediated cell death by inhibiting the NLRP3 signaling pathway. Collectively, these findings suggest that inhibiting ceramide synthase 5 expression in microglia after spinal cord injury effectively suppressed microglial pyroptosis mediated by NLRP3, thereby exerting neuroprotective effects.

01 Feb 2025·JOURNAL OF LIPID RESEARCH

Contribution of individual phospholipase A2 enzymes to the cleavage of oxidized phospholipids in human blood plasma

Article

Author: Fedorova, Maria ; Oskolkova, Olga ; Jokesch, Philipp ; Gesslbauer, Bernd ; Bochkov, Valery

Phospholipids containing oxidized esterified PUFA residues (OxPLs) are increasingly recognized for multiple biological activities and causative involvement in disease pathogenesis. Pharmacokinetics of these compounds in blood plasma is essentially not studied. Human plasma contains both genuine phospholipases A₂ [platelet activating factor acetyl hydrolase (PAF-AH) (also called Lp-PLA₂) and secretory phospholipase A2] and multifunctional enzymes capable of removing sn-2 residues in native and oxidized PLs (lecithin-cholesterol acyltransferase, peroxiredoxin-6). The goal of this study was to compare relative activities of different PLA₂ enzymes by analyzing cleavage of oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylcholine (OxPAPC) and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylethanolamine (OxPAPE) by diluted plasma in the presence of enzyme inhibitors. We have found that human plasma demonstrated high total PLA₂ activity against oxidized PCs and PEs. PAF-AH/Lp-PLA₂ played a dominant role in LysoPC and LysoPE production as compared to other enzymes. Molecular species of oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylcholine and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylethanolamine could be divided into three groups according to their degradation rate and sensitivity to PAF-AH/Lp-PLA₂ inhibitor darapladib. Oxidatively truncated species were most rapidly metabolized in the presence of plasma; this process was strongly inhibited by darapladib. The rate of degradation of full-length OxPLs depended on the degree of oxygenation. Species containing 1 to 3 oxygen atoms were relatively stable to degradation in plasma, while OxPLs containing > 3 extra oxygens were degraded but at significantly slower rate than truncated species. In contrast to truncated species, degradation of full-length OxPLs with > 3 extra oxygens were only minimally inhibited by darapladib. These data provide further insights into the mechanisms regulating circulating levels of OxPLs and lipid mediators generated by PLA₂ cleavage of OxPLs, namely oxylipins and LysoPC.

01 Jan 2025·JOURNAL OF LIPID RESEARCH

Identification of plasma proteins binding oxidized phospholipids using pull-down proteomics and OxLDL masking assay

Article

Author: Übelhart, Rudolf ; Bochkov, Valery ; Jantscher, Lydia ; Guttzeit, Sebastian ; Oskolkova, Olga ; Jokesch, Philipp ; Holzer, Lisa ; Bochkov, Valery B. ; Gesslbauer, Bernd

Oxidized phospholipids (OxPLs) are increasingly recognized as toxic and proinflammatory mediators, which raises interest in the mechanisms of their detoxification. Circulating OxPLs are bound and neutralized by plasma proteins, including both antibodies and non-immunoglobulin proteins. The latter group of proteins is essentially not investigated because only three OxPC-binding plasma proteins are currently known. The goal of this work was to characterize a broad spectrum of plasma proteins selectively binding OxPLs. Using pull-down-proteomic analysis, we found about 150 non-immunoglobulin proteins preferentially binding oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylcholine (OxPAPC) as compared to non-oxidized PAPC. To test if candidate proteins indeed can form a barrier isolating OxPLs from recognition by other proteins, we applied an immune masking assay. Oxidized LDL (OxLDL) immobilized in multiwell plates was used as a carrier of OxPLs, while mAbs recognizing OxPC or OxPE were used as "detectors" showing if OxPLs on the surface of OxLDL are physically accessible to external binding partners. Using an orthogonal combination of pull-down and masking assays we confirmed that previously described OxPL-binding proteins (non-fractionated IgM, CFH, and Apo-M) indeed can bind to and mask OxPC and OxPE on liposomes and OxLDL. Furthermore, we identified additional plasma proteins selectively binding and masking OxPC including Apo-D, Apo-H, pulmonary surfactant-associated protein B, and antithrombin-III. We hypothesize that in addition to circulating antibodies, multiple non-immunoglobulin plasma proteins can also bind OxPLs and modulate their recognition by innate and adaptive immunity.

News (Medical) associated with Darapladib

08 Jul 2024

·www.prnewswire.com

DP Technology Announces Nomination of Development Candidate, a Potential Best-in-Class Lp-PLA2 Inhibitor for DR and DME

The nomination of novel Lp-PLA2 inhibitor DPT0415 for the treatment of DR & DME. DPT0415 is a highly potent, selective and safe Lp-PLA2 inhibitor with sufficient target engagement at a dose of 0.3 mpk and robust efficacy in the STZ-induced rat DR model. This project further validates the capabilities of DP Technology's drug design platform RiDYMO. BEIJING, July 8, 2024 /PRNewswire/ -- DP Technology, an "AI for Science" paradigm-driven company, today announced the nomination of DPT0415, a novel small molecule targeting Lipoprotein‐associated phospholipase A2 (Lp-PLA2), as a preclinical candidate compound for the treatment of diabetic retinopathy (DR) and diabetic macular edema (DME). Continue Reading Lp‐PLA2 belongs to group VII of the PLA2 superfamily, primarily secreted by macrophages and circulates in the blood as a complex with low‐density lipoprotein (LDL) and high‐density lipoprotein (HDL)[1]. Lp-PLA2 hydrolyzes oxidized phospholipids, typically on low-density lipoprotein (LDL) to generate lysophosphatidylcholine (lysoPC). LysoPC induces vascular inflammation, leading to damage to the blood-retinal barrier (BRB)[2]. DR is a microvascular complication of diabetes and a major cause of vision loss in middle-aged and elderly people. One-third of people with diabetes have DR[3]. DME can occur at any stage of DR, which is caused by excess fluid and lipid accumulation in the macula due to a breakdown in the blood-retinal barrier. When the edema extends into the fovea, the patient becomes symptomatic with metamorphopsia and vision loss[4]. The advent of intraocular anti-vascular endothelial growth factor (anti-VEGF) drugs has revolutionized the treatment of DME. However, many patients with DME do not show complete resolution of fluid despite multiple injections[5], probably because DR is also an inflammatory disease with many cytokines and chemokines involved in the process[6]. Thus, the molecular mechanisms beyond VEGF should be explored. As a Lp-PLA2 inhibitor, oral administration of Darapladib modestly reduced edema and improved vision in a center-involved DME phase IIa study[7]. DPT0415 is a highly potent, selective and safe Lp-PLA2 inhibitor with a novel scaffold. It demonstrated sufficient target engagement at 0.3 mpk, and resecured retinopathy in the STZ-induced rat DR model. The compound exhibits higher potency, better ADME and physicochemical properties than Darapladib, and demonstrated sufficient safety margin in preclinical studies. "The current standard of care for DME requires eye injections of VEGF antibody to preserve vision. Due to the invasive route of administration, patients tend to delay treatment until the later stages of the disease." said Xiaomin Zhang, Head of Drug Discovery at DP Technology. "As an oral therapy for the treatment of DR & DME, DPT0415 may address inflammation and vascular leakage to improve vision by targeting Lp-PLA2. Furthermore, the Lp-PLA2 inhibitor DPT0415 has the potential to substantially change the therapeutic paradigm by treating DR at an earlier stage to achieve better outcomes." "DP Technology is the pioneer of the AI for Science paradigm, dedicated to integrating 'AI + Simulation + Experiments' to address unmet medical needs," said Weijie Sun, Founder and CEO of DP Technology. "The successful discovery of DPT0415 is empowered by multiple modules such as Uni-FEP and Uni-QSAR in the RiDYMO® platform to optimize potency and ADME properties. These practical applications of algorithms represent an important step towards realizing the vision of AI for Science. We look forward to collaborating with seasoned partners to advance this program to the next milestone." The RiDYMO® drug design platform integrates various AI and physical algorithms, dedicated to the development of drugs for "undruggable" targets and "best-in-class" molecules. As one of its core algorithms, Reinforced Dynamics (RiD) has a significant advantage in the sampling efficiency of molecular dynamics simulation. By fully leveraging the high-dimensional representation capabilities of neural networks, RiD can efficiently capture dynamic conformational changes in complicated biomolecular systems. The RiDYMO® platform is dedicated to studying the dynamics of biological systems and revealing cryptic binding sites, encompassing a range of challenging systems including protein-protein interactions (PPIs), intrinsically disordered proteins (IDPs), membrane proteins, RNA, and others. Its effectiveness has been confirmed through validation on challenging targets, including the c-Myc protein, c-Myc RNA, GPX4 protein, Kv1.3 protein, and others. About DP Technology DP Technology, an "AI for Science" new paradigm-driven company, dedicated to applying Artificial Intelligence and Molecular Simulation algorithms to solve important scientific problems by combining advanced computational methods. Relying on DP Technology's Dynamics-based drug design platform, RiDYMO®, we have set up a world-leading hit discovery platform. The team has established external collaborations and built up strong internal pipeline, focusing on three areas of CNS, oncology and autoimmune diseases. For collaboration and further information，please contact Dr. Xiaomin Zhang, [email protected]. References: 1. Curr. Pharm. Des. 20, 6256-6269 (2014). 2. Arterioscler. Thromb. Vasc. Biol. 25, 923-931 (2005). 3. Diabetes Care 35, 556-564 (2012). 4. Ophthalmology 122, 1375-1394 (2015). 5. Ophthalmology 117, 1064-1077 (2010). 6. Semin. Immunopathol. 30, 65-84 (2008). 7. Ophthalmology 122, 990-996 (2015). SOURCE DP Technology

Clinical ResultPhase 1Phase 2

20 Jan 2017

·www.biospace.com

New FDA Report Cites 22 Drugs That Passed Phase II But Crashed and Burned in Phase III

January 20, 2017 By Mark Terry , BioSpace.com Breaking News Staff The Trump administration has indicated plans to reform the U.S. Food and Drug Administration (FDA) “to put greater focus on the need of patients for new and innovative medical products.” So far, it hasn’t selected a commissioner for the FDA, although some of the names suggested, such as Jim O’Neil , a venture capitalist, and Balaji Srinivasan , co-founder of genetics testing company Counsyl , have showed indications that they want to focus on drug safety rather than efficacy, perhaps even cutting the need for in-depth Phase III clinical trials. The FDA just published a study titled, “22 Case Studies Where Phase 2 and Phase 3 Trials Had Divergent Results .” Below are the so-called Hall of Shame drugs that showed promise in Phase II, but failed in Phase III. 1. Bitopertin ( Roche , . For schizophrenia. Failed to improve the negative symptoms of schizophrenia. 2. Bitopertin ( Bristol-Myers Squibb , . For hepatocellular cancer. Failed to improve overall patient survival compared to approved treatment and had unexpected toxicities. 3. Capsaicin Topical Patch, Qutenza ( NeurogesX , ). To treat HIV-associated nerve pain, with previous approval for treatment of shingles-associated nerve pain. Lack of efficacy compared to control groups. 4. Darapladib ( GlaxoSmithKline , .) As an add-on to statins for cardiovascular disease in patients with a prior heart attack. Failed for lack of efficacy, despite promising biomarker evidence in Phase II. 5. Dexmecamylamine ( Targacept , / AstraZeneca , . For add-on treatment of depression. No more effective than placebo in Phase III trials for treatment of depression. 6. Exhale Drug-Eluting Stent ( Broncus Technologies ). For reduction of shortness of breath in emphysema patients. Statistically significant results in Phase II, but failed to improve lung function or symptoms in Phase III. 7. Experimental HSV-2 Vaccine ( Chiron , now Novartis Vaccines & Diagnostics ). To prevent genital herpes. Positive biomarker results in Phase II, did not prevent genital herpes in Phase III. 8. Gluatmic Acid Decarboxylase Vaccine ( Diamyd Medical ). For the preservation of insulin secretion for patients with recent-onset type 1 diabetes. Promising results in Phase II, but in the Phase III trial, did not improve pancreatic function or clinical outcomes. 9. Imiquimod, Aldara 5% Cream ( 3M , . To treat molluscum contagiosum (MC) lesions in children. Was approved to treat external anogenital warts. Showed promising Phase II results, but in Phase III did no better than placebo. 10. Iniparib ( Sanofi , . As an add-on treatment of triple negative breast cancers. Showed promising tumor response and survival in Phase II, but in Phase III did not improve survival. 11. Lithium ( King’s College London , UK). Already a treatment for bipolar disorders, was being tested as an add-on treatment to delay disease progression of amyotrophic lateral sclerosis. Showed positive effects on disease progression and survival in Phase II, but in Phase III did not improve survival, health status or quality of life. 12. MAGE-A3 Vaccine ( GlaxoSmithKline , . For non-small cell lung cancer (NSCLC). Proof of concept trial was promising, but showed no clinical benefit compared to placebo in Phase III. 13. NicVAX Vaccine ( Nabi Biopharmaceuticals , . For smoking cessation. Promising Phase II, but in Phase III the abstinence rate was similar to placebo. 14. Velimogene Aliplasmid, Allovectin-7 ( Vical , . For metastatic melanoma. In Phase II, showed evidence of tumor shrinkage. In Phase III, reduced tumor size in significantly fewer patients than two other marketed drugs. 15. Olanzapine Pamoate, Zyprexa Relprevv ( Eli Lilly , . Evaluated for long-acting injection treatment for schizophrenia. Already approved as an oral short-acting treatment for schizophrenia. In Phase III, identified serious safety risks. 16. Aliskiren, Rasilez, Tekturna ( Novartis , . Evaluated as an add-on treatment for prevention of congestive heart failure (CHF) complications. Previously approved for hypertension. Positive results in an proof of concept study, but in the Phase III trial adding aliskirin to standard therapy, did not cut cardiovascular-related death or CHF re-hospitalization, and showed an increase in kidney failure and low blood pressure. 17. CoStar Drug-Eluting Stent ( Conor Medsystems ). To cut heart attack risk in patients with coronary artery disease. Although approved in Europe and had positive results in a small trial, patients who received it in Phase III trials had worse outcomes than those receiving different stents. 18. Figitumumab ( Pfizer , . Evaluated as an add-on treatment of advanced non-small cell lung cancer (NSCLC). Showed promise in Phase II, but in Phase III failed to improve survival. Also, in one combination with another regimen, increased serious adverse events and deaths. 19. Recombinant Factor VIIa, NovoSeven ( Novo Nordisk , . Evaluated for decrease of intracerebral bleeding and hematoma size in stroke patients. Already approved for hemophilia. Showed positive Phase II results, but in Phase III, patients didn’t show clinical benefits, but did have an increase incidence of serious events compared to patients receiving the placebo. 20. Semagacestat ( Eli Lilly , . For Alzheimer’s disease. Showed promising biomarker results in Phase II, but the Phase III trial was ended early because patients receiving the drug had worsened cognition, worse functional status, and an increased risk of skin cancer. 21. Torcetrapib ( Pfizer , . For the prevention of cardiovascular events in patients with a history of cardiovascular disease or type 2 diabetes. Showed improved cholesterol levels in Phase II trials, but in Phase III it increased mortality and cardiac events compared with placebo. 22. V710 Vaccine (Intercell--now Valneva / Merck , . V710 Vaccine (Intercell (now Valneva)/Merck, MRK). Evaluated as a vaccine to prevent Staphylococcus aureus infection. Showed promise in Phase II, but the Phase III clinical trial was ended early because of lack of efficacy and the potential risk for serious adverse events and death. John Carroll , writing for Endpoints News, writes , “Some on the libertarian side have said they want to simply toss out the gold standard on efficacy and safety altogether, excoriating the old rules of market engagement. That toxic argument raises some important questions about each stage of drug development. And there’s a new report out from the FDA that covers just what you can miss if you cut Phase III out altogether.”

Clinical ResultPhase 3Phase 2VaccineDrug Approval

26 Oct 2016

·www.biospace.com

GlaxoSmithKline Terminates Development of Losmapimod for COPD

October 26, 2016 By Alex Keown , BioSpace.com Breaking News Staff LONDON – One year after Losmapimod finally flunked out as a treatment for high-risk heart disease patients, GlaxoSmithKline pulled the plug on the drug as a potential treatment for patients with COPD. GSK’s decision came following a long and hard look at Phase II data, according to an Endpoints report. Losmapimod is a selective inhibitor of the enzyme family known as p38 mitogen-activated protein kinases, which are mediators of acute inflammation. GSK has a number of treatments for COPD in its pipeline, but the loss of the Losmapimod program will be another sour note for Andrew Witty as he closes out his tenure at the helm of the company. There had been hopes that Losmapimod would be a strong performer for GSK, but that was not to be the case. In January 2016, GSK pulled the plug on another Phase III trial with Losmapimod for acute myocardial infarcation (heart attack) after disappointing trial results were announced. GlaxoSmithKline has had a tough go in recent years with some of its R&D efforts. In 2014 another heart drug, darapladib, dialed to meet primary endpoints in a Phase III trial. Still, while the Losmapimod failure is disappointing for a company looking to drum up excitement about its R&D pipeline, the company did see a strong 23 percent surge in sales during the third quarter to $9.8 billion, according to its report. Sales were driven, in part by its respiratory drugs Revlar/Breo, Anoro, Incruse and Nucala, the company said. The company was also bolstered by the filing of its New Drug Application in the United States for Shingrix, a shingles treatment. Witty said the quarter reflected strong performances across the company. With the filing for Shingrix, Witty said the company has completed three of four NDAs in the U.S. the company targeted for the second half of 2016. Additionally, he said the company has launched four Phase III trials for HIV, respiratory and anemia treatments, as well as five Phase II trials. Still, the company is looking for a turnaround in sales, which were rather flat last year in Europe and the U.S. In the U.S., sales were down about 10 percent as the result of formulary and contract changes to asthma drug Advair. Glaxo is under pressure to develop new drugs that aren’t threatened by generics. Earlier this year, Witty had announced his intention to step down in March 2017, after 10 years atop the company. His resignation comes at a time when investors have questioned company strategy to combat lagging sales, as well as several scandals that rocked the company. In September, GSK tapped Emma Walmsley to helm the company. She will move to the CEO slot after spending time running the company’s consumer healthcare division.

Executive ChangePhase 2Phase 3

100 Deals associated with Darapladib

External Link

KEGG	Wiki	ATC	Drug Bank
D03650	Darapladib	-	DB06311

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Coronary Artery Disease	Phase 3	United States	GSK Plc	04 Feb 2010
Endothelial dysfunction	Phase 3	United States	GSK Plc	04 Feb 2010
Acute Coronary Syndrome	Phase 3	United States	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	China	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Japan	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Argentina	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Australia	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Belgium	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Brazil	GSK Plc	01 Dec 2009
Acute Coronary Syndrome	Phase 3	Bulgaria	GSK Plc	01 Dec 2009

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00268996 (CTgov)	Phase 2	Atherosclerosis \| Coronary Disease	336	placebo (Placebo)	jdhkixdvhb(jpowdkjtvp) = yqsuivgwgt gtangqupoj (kdbzdfnhkc, vxnjywgyeq - ayjrcktdnp) View more	-	19 Feb 2018
				Darapladib (Darapladib 160 mg EC Tablet)	jdhkixdvhb(jpowdkjtvp) = mxmdaawhwf gtangqupoj (kdbzdfnhkc, phblxasuqh - obxhxweyra) View more
NCT00734032 (CTgov)	Phase 2	Atherosclerosis	107	placebo (Placebo)	rxnbauaqhj(tgygubtbqn) = szaeljqyfs khkcnysgbr (rthwazufxb, 8.5) View more	-	12 Jan 2018
				SB-480848 (SB-480848 40 mg)	rxnbauaqhj(tgygubtbqn) = xcgaqkbimo khkcnysgbr (rthwazufxb, 24.6) View more
NCT00799903 (STABILITY \| 100601, CTgov)	Phase 3	Plaque, Atherosclerotic \| Coronary Disease	15,828	Placebo (Placebo)	djfbfnbgxp = ekfaqodsvo mahngcrqwm (rywnmgwbyz, hvqrbdridn - kfdxsdnszv) View more	-	10 Aug 2017
				Darapladib (Darapladib)	djfbfnbgxp = eqctunimwy mahngcrqwm (rywnmgwbyz, qpusekmskl - tbnztmnjjp) View more
NCT01000727 (SOLID-TIMI 52, CTgov)	Phase 3	Acute Coronary Syndrome \| Myocardial Infarction	13,026	Placebo (Placebo)	giobyvbwqw = iwoswahcoh gukshtjyfs (mmfhlwgsps, akzutknckf - wgxwkkxini) View more	-	10 Aug 2017
				Standard Therapy+Darapladib 160 mg (Darapladib 160 mg)	giobyvbwqw = tteuydgwid gukshtjyfs (mmfhlwgsps, xnkuccgqkf - udujtugmes) View more
NCT01067339 (CTgov)	Phase 3	Coronary Artery Disease \| Endothelial dysfunction	70	darapladib (Darapladib)	hddvgpiotf(qzdkdqmezs) = ukjdmqokas fozpogelze (verulsxmlu, xcvpqedsyg - hlrcsoyjgt) View more	-	15 Mar 2017
				placebo (Placebo)	hddvgpiotf(qzdkdqmezs) = gghrzqipkr fozpogelze (verulsxmlu, agbmchiyiu - jvbthfnttu) View more
NCT02000804 (Pubmed \| PLoS One)	Phase 1	lipoprotein-associated phospholipase A2	-	Darapladib 160 mg	sebovjolwl(dwovrpecax) = fknnbkketi dqizmmydjv (birskzjyrh, 49.9%) View more	-	14 Oct 2015
NCT01000727 (SOLID-TIMI 52, Pubmed \| JAMA)	Phase 3	Acute Coronary Syndrome	13,026	Darapladib	jttrvxdsyu(qytilbhqdk) = yvhbdkjalp djygbmbyvq (fcgzpkjwga ) View more	Negative	10 Sep 2014
				Placebo	jttrvxdsyu(qytilbhqdk) = usjwsqosdm djygbmbyvq (fcgzpkjwga ) View more
PO201 (AAO2013)	Phase 2	Diabetic macular oedema	-	Darapladib	acmhlgthge(rntnjztgxc) = omepnqpzcq zmvwiohgbl (rtegztxuhz, 2.3 - 5.8) View more	Positive	17 Nov 2013

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