HCAR3 agonists(HM74 nicotinic acid GPCR agonists), NIACR1 agonists(Hydroxycarboxylic acid receptor 2 agonists), PGD2 receptor antagonists(Prostaglandin D2 receptor antagonists)

Therapeutic Areas

Endocrinology and Metabolic DiseaseCardiovascular DiseasesCongenital Disorders+ [1]

Active Indication-

Inactive Indication

AtherosclerosisCombined hyperlipidemiaDiabetes Mellitus, Type 2+ [7]

Originator Organization

Merck Sharp & Dohme Corp.

Active Organization-

Inactive Organization

Merck Sharp & Dohme Corp.Merck Sharp & Dohme Ireland Ltd.Merck GmbH

Drug Highest PhaseWithdrawn

First Approval Date

EU (03 Jul 2008),

DyslipidemiasPrimary hypercholesterolemia

Regulation-

Structure

Molecular FormulaC27H24ClFN2O6S

InChIKeyZZRFQBQNZLFESZ-BTQNPOSSSA-N

CAS Registry1046050-73-0

Clinical Trials associated with Laropiprant/Nicotinic Acid

NCT03540758 / RecruitingPhase 2IIT

Regulation of Endogenous Glucose Production by Central KATP Channels

Type 2 diabetes affects the ability of the body to process glucose (sugar). Under fasting conditions, the liver is able to make sugar to maintain glucose levels in an important process called endogenous glucose production (EGP). Previous studies suggest that the central nervous system (CNS), including the brain, helps to regulate levels of glucose in the body by communicating with the liver. This process can be impaired in people with type 2 diabetes, and can contribute to the high level of glucose seen in these individuals.
The purpose of this study is to understand how activating control centers of the brain with a medication called diazoxide can affect how much glucose (sugar) is made by the liver. This is particularly important for people with diabetes who have very high production of glucose, which in turn can lead to diabetes complications.

Start Date01 Aug 2018

Sponsor / Collaborator

Albert Einstein College of Medicine, Inc.

[+2]

EUCTR2014-003213-29-PL / Unknown statusNot ApplicableIIT

A randomized, multicenter, open-label, two-arm, parallel, phase III study to evaluate the efficacy and safety of nicotinic acid administered in combination with simvastatin for 6 months in comparison to simvastatin therapy alone in inhibiting the progression of atherosclerosis in patients with carotid arteries stenosis and dyslipidemia.

Start Date02 Mar 2015

Sponsor / Collaborator-

NCT01683656 / TerminatedPhase 4IIT

ER Niacin/Laropiprant Impact on Cardiovascular Markers and Atheroprogression in HIV-infected Individuals on cART

HIV-infected patients are at increased risk for cardiovascular disease. Large investigations support an inverse correlation between HDL-C levels and coronary heart disease. Therefore a treatment lowering HDL-C such as niacin could reduce the risk of atheroprogression not only through its benefit in terms of lipid profile, but also by reducing atherosclerotic inflammation.
The study aims at showing that a therapy targeting HDL-C increase in HIV-infected patients on suppressive cART has the potential for reducing subclinical atherosclerotic inflammation associated with HIV itself in HIV-individuals on cART.
NILACH is a randomised, multicenter, double blind, placebo controlled, 48 weeks trial to test the effect of the newly marketed niacin/laropiprant on carotid intima-media thickness (IMT) in 90 subjects.
Regimen 1: ER niacin/laropiprant 1g/20 mg for the first 4 weeks and 2g/40mg from week 5 to the end of the study (the titration aims to reduce adverse reactions)
Regimen 2: ER niacin/laropiprant placebo p.m.
The primary end point is the change in mean common carotid intima-media thickness from baseline and 48 weeks, compared between the niacin/laropiprant group and the placebo group.
The proposed in vivo experiments should provide insights on the potential benefits of niacin treatment of cardiovascular disease in HIV patients. In addition, we will be able to further clarify the role of systemic inflammatory mediators in the development of early atherosclerosis of HIV-infected patients on antiretroviral therapy. Detection and treatment of non-infectious co-morbidities such as cardiovascular diseases have become essential for HIV-infected individuals exposed to lifelong antiretroviral therapy and go beyond mere management of opportunistic infections or virologic suppression.

Start Date01 Aug 2012

Sponsor / Collaborator

Les Hôpitaux Universitaires de Genève

[+3]

100 Clinical Results associated with Laropiprant/Nicotinic Acid

100 Translational Medicine associated with Laropiprant/Nicotinic Acid

100 Patents (Medical) associated with Laropiprant/Nicotinic Acid

306

Literatures (Medical) associated with Laropiprant/Nicotinic Acid

01 Dec 2024·ENVIRONMENTAL RESEARCH

Effects of trehalose and sodium alginate on microbially induced carbonate precipitation

Article

Author: Luo, Weijun ; Zhou, Limin ; Zheng, Xiangmin ; Yu, Wenwen ; Zhang, Lidong ; Huang, Xiaowen

The process of altering the microbial-induced carbonate precipitation (MICP) by adding additives has been extensively studied. The impact of polysaccharides, as an important component of bacteria, still requires deeper exploration on MICP. This work thus focuses on two types of sugars, sodium alginate (SA) and trehalose (Tre), to explore their effects on biomineralization of carbonate induced by Bacillus pumilus Z6. The results show that B. pumilus Z6 can raise the environmental pH and increase the supersaturation of carbonate and bicarbonate ions through carbonic anhydrase. The presence of organic functional groups and the negative carbon isotope signatures in minerals provide evidence of microbial involvement. Tre and SA do not change the mineral phase, which mainly consists of hollow rice-like granular vaterite and irregular calcite. Tre is conducive to the formation of calcite, whereas the carboxyl groups in SA contribute to the stability of vaterite. Both Tre and SA enhance the removal rate of calcium ions; however, SA is more effective for this purpose. Furthermore, mineralization experiments with calcium alginate gel tablets indicate that SA can attract calcium carbonate to nucleate on its surface. This research offers significant insights into biomineralization processes and introduces novel perspectives for advancing MICP technology.

01 Nov 2024·Pediatric Obesity

Effects of 8‐h time‐restricted eating on energy intake, dietary composition and quality in adolescents with obesity

Article

Author: Salvy, Sarah Jeanne ; Vu, My H. ; Bakhsh, Jomanah A. ; Goran, Michael I. ; Vidmar, Alaina P.

Summary:

Background:

The precise mechanisms underlying the health benefits of time‐restricted eating (TRE) are unclear, particularly in adolescents.

Objectives:

This secondary analysis examines the impact of 8‐h TRE on energy intake, dietary composition and quality in adolescents with obesity, using data from a 12‐week randomized, controlled pilot trial.

Methods:

Participants (14–18 years with BMI >95th percentile) were assigned to either 8‐h TRE with real‐time or blinded continuous glucose monitoring or a control group with a 12+ h eating window. Dietary intake was analysed using the Nutrient Data System Recall 24‐h Dietary Recall and the Healthy Eating Index (HEI‐2020) for assessing diet quality.

Results:

The study included 44 participants (32 TRE, 12 control), predominantly female and Hispanic/Latino. The TRE group showed a significant reduction in mean energy intake (−441 kcal/day), carbohydrates (−65 g/day), added sugar (−19 g/day) and fat (−19 g/day), while the control group had a similar reduction in energy intake (−437 kcal/day) and carbohydrates (−63 g/day), but no significant changes in added sugar or fat. The percent energy intake from protein increased more in the TRE group compared to the control. The TRE group experienced a significant improvement in diet quality, with a 6.3‐point increase in HEI‐2020 score; however, between‐group comparisons were not statistically significant.

Conclusion:

There were no significant differences between the TRE and control groups in energy intake, dietary composition or quality. Future research with larger sample sizes is needed to further evaluate the potential impact of TRE on dietary behaviours.

01 Oct 2024·DIABETES OBESITY & METABOLISM

The effects of time‐restricted eating alone or in combination with probiotic supplementation in comparison with a calorie‐restricted diet on endocrine and metabolic profiles in women with polycystic ovary syndrome: A randomized clinical trial

Article

Author: Djafarian, Kurosh ; Shab‐Bidar, Sakineh ; Talebi, Sepide ; Mohammadi, Hamed ; Moini, Ashraf

Abstract:

Aim:

To assess the impact of intermittent fasting, with or without probiotic supplementation, versus a calorie‐restricted diet on anthropometric measures, metabolic status and gonadal variables in women with polycystic ovary syndrome (PCOS).

Methods:

This is a randomized, placebo‐controlled, parallel‐arm clinical trial. The effects of the 14:10 early time‐restricted eating (eTRE) strategy alone or combined with probiotics, on obese women with PCOS, were investigated. Participants were divided into three groups: eTRE plus probiotics (n = 30), eTRE plus placebo (n = 30) and a control group following a standard three‐meal‐per‐day diet with daily calorie restriction (DCR) (n = 30). Over 8 weeks, various anthropometric, metabolic, menstrual and gonadal variables were assessed.

Results:

A total of 90 individuals were included in the study, with a mean body weight of 81.4 kg, and a mean age of 30 years. Mean (standard deviation) weight loss was not different between the groups at week 8 (TRE + probiotic: −2.2 [1.6] kg vs. TRE + placebo: −2.9 [2.7] kg vs. DCR: −2.5 [1.7] kg). Results revealed that, while all three regimes led to reductions in body weight, body mass index, vascular risk indicators, hirsutism and acne scores, there were no statistically significant differences between the eTRE groups and the control group in terms of weight loss, or improvements in metabolic, menstrual and gonadal variables (P > .05). Additionally, combining probiotics with eTRE did not benefit hormonal and cardiometabolic factors (P > .05).

Conclusions:

The eTRE alone or eTRE plus probiotics did not result in significantly greater weight loss or improvements in metabolic, menstrual and gonadal variables compared with the standard three‐meal DCR diet.

News (Medical) associated with Laropiprant/Nicotinic Acid

08 Apr 2021

·medcitynews.com

Ventus Therapeutics tacks on $100M to take on ‘undruggable’ disease targets

In the span of one year, Ventus Therapeutics has developed a new technology that figures out how to get small molecules to bind to proteins previously deemed “undruggable.” The startup has also grown its pipeline from three programs to five, two of which are on track for clinical testing. Ventus, which has operations in Waltham, Massachusetts and Montreal, now has $100 million in additional financing. But here’s the thing: It doesn’t need the money. The startup still has more than half of the $60 million in Series A cash it raised when it emerged from stealth last year, said CEO Marcelo Bigal. What the new cash will enable it to do is to work on all five drug programs instead of picking and choosing which ones to prioritize. “The money gives me the runway that I need to do this,” Bigal said. “It also gives me the balance sheet if I want to do something different, like an IPO.” The Series B round of funding announced Thursday was led by RA Capital Management. Ventus launched last year with technology that enables scientists to understand the structure of innate immune system proteins. With that knowledge, the company discovers small molecules that can target these proteins. Ventus still has this structural immunology platform, but it has since developed additional technology that enables it to see the pockets on a protein that are druggable by small molecules. Unlike the company’s first technology, it’s not limited to innate immune system proteins. The new Ventus technology, called ReSOLVE, accounts for how proteins move and change shape. As proteins move, druggable pockets will be visible only in some conformations, Bigal said. ReSOLVE enables scientists to see where and when a protein’s druggable pockets are accessible. Ventus isn’t the only startup that has developed technology that accounts for protein motion. But Bigal added that there’s more to the technology, and it’s reflected in its name. “SOLVE” isn’t a suggestion that the technology solves a problem, rather, it’s meant to convey “solution,” as in water. Cells are filled with fluid, and that fluid affects how proteins move. “We account for how the water dynamics change the druggable pockets,” Bigal said. Ventus is using its technology to develop drugs for autoimmune diseases, inflammatory disorders, and cancer. The company isn’t yet revealing specific disease targets. But the company has disclosed that its second most advanced small molecule, stemming from its initial innate immune system research, targets NLRP3. That protein is an inflammasome—it mediates pro-inflammatory cytokine proteins IL-1b and IL-18. NLRP3 is linked to many autoimmune diseases characterized by inflammation. It’s a target of interest for several companies and has been the basis of several deals in recent years. In 2018, Genentech paid an undisclosed amount to acquire pre-clinical stage Jecure Therapeutics and its pipeline of NLRP3 inhibitors. In 2019, Novartis paid $310 million up front to acquire IFM Tre, whose lead NLRP3 program at the time was in early clinical development for the liver disorder nonalcoholic steatohepatitis as well as other inflammatory diseases. Last June, NodThera raised $55 million in Series B cash to support its work developing NLRP3 inhibitors for chronic inflammation disorders. The company’s lead NLRP3 inhibitor is in early-stage clinical testing and the pipeline includes compounds that can cross the blood-brain barrier. Using its protein structure technologies, Ventus says it was able to understand the dynamics of NLRP3’s binding pocket. From there, the company identified and optimized small molecules to bind to those pockets. These molecules include ones capable of penetrating into the brain, and Bigal said Ventus will pursue neurological disorders as well as systemic diseases. The two lead Ventus programs should yield drug candidates by the first quarter of next year, and then enter clinical testing by the end of 2022, Bigal said. Bigal said that Ventus’s protein technologies are capable of developing dozens of drugs—much more than a young company can handle on its own. But Ventus won’t be adding compounds to its pipeline, at least in the near term. The company is exploring potential partnerships with larger pharmaceutical companies. Bigal said he’s not looking for partners that want to develop Ventus’s internal pipeline. Instead, he’d like to strike deals with companies that want to use the startup’s technology to develop drugs for other diseases. With Ventus’s new financing, Josh Resnick, managing director at RA Capital, will join the Ventus board of directors. The Ventus financing marks the second time in as many days that RA Capital has splashed out cash for a company bound for the clinic. The investment firm also led the $100 million Series B round of funding that Seattle-based Icosavax announced on Wednesday. The latest Ventus financing included the participation of BVF Partners, Casdin Capital, Cormorant Asset Management, Fonds de solidarité FTQ, and Alexandria Venture Investments. Versant Ventures, the venture capital firm that founded Ventus, also invested, as did GV, another earlier investor. Photo by Ventus Therapeutics

Small molecular drugIPO

28 Mar 2019

·www.biospace.com

IFM Therapeutics Announces Dosing of First Subjects in Phase 1 Healthy Volunteer Study of Lead NLRP3 Antagonist, IFM-2427

Announcement marks first human trial for an NLRP3 antagonist BOSTON, March 28, 2019 /PRNewswire/ -- IFM Therapeutics (IFM), a privately held biopharmaceutical company focused on developing therapies that modulate novel targets in the innate immune system, today announced that the first subjects have been dosed in a Phase 1 healthy volunteer trial of IFM-2427. IFM-2427, the lead program from IFM's subsidiary IFM Tre, is a first-in-class systemic NLRP3 (NOD-, LRR- and pyrin domain-containing 3) antagonist that can potentially block the inflammatory responses underlying a variety of serious diseases. "Initiating this Phase 1 trial of IFM-2427 – less than a year after IFM Tre was launched – is a meaningful achievement for IFM and reflective of our team's ability to efficiently advance product candidates from discovery to clinical development," said Gary D. Glick, Ph.D., Chief Executive Officer and Co-Founder of IFM Therapeutics. "Further, this first-in-human study of a systemic NLRP3 inhibitor reinforces our leadership in innate immune system biology. We are committed to exploiting the full therapeutic potential of NLRP3 inhibition through the advancement of chemically-distinct molecules with varying mechanisms of action and across a breadth of indications." NLRP3 is an intracellular innate immune signaling receptor that allows immune cells to detect the presence of pro-inflammatory foreign or endogenous molecules that signal infection, tissue damage or metabolic derangements. These conditions trigger the assembly of a multi-protein complex called an inflammasome, which then initiates an immune response. While this response can be useful for fending off foreign pathogens, abnormal or chronic activation of the NLRP3 inflammasome is known to cause negative downstream effects and the onset and progression of numerous diseases. IFM-2427 is the first of IFM Tre's three unique development candidates to enter the clinic, all of which are intended to block only the inflammation driven by the NLRP3 pathway, leaving other immune pathways unsuppressed and free to produce inflammatory responses to confront harmful pathogens. IFM-2427 is a first-in-class small molecule designed to inhibit the activity of NLRP3 outside the central nervous system by directly binding to the protein, thereby blocking its activation that leads to the maturation of the pro-inflammatory cytokines IL-1, IL-18 along with pyroptosis, an inflammatory form of cell death. The Phase I clinical study of IFM-2427 is being carried out in up to 90 subjects and is expected to complete in the fourth quarter of 2019. About IFM Tre IFM Tre, a subsidiary of IFM Therapeutics (IFM), is a biopharmaceutical company developing a suite of small-molecule antagonists targeting inappropriate inflammatory responses of the innate immune system via the NLRP3 pathway, which is believed to underlie a variety of serious diseases. The Company is developing chemically distinct systemic, gut-directed and CNS-penetrant drug candidates to address a breadth of indications triggered by NLRP3, including metabolic, fibrotic, autoimmune, autoinflammatory, and neurodegenerative diseases. About IFM Therapeutics IFM Therapeutics (IFM) is a privately held biopharmaceutical company based in Boston, Massachusetts. The Company was founded by an international group of preeminent scientists and physicians following the sale of IFM Therapeutics, Inc (originally founded by Gary Glick and Atlas Venture) to Bristol-Myers Squibb. IFM's team has discovered and developed small molecules that modulate novel targets in the innate immune system as next-generation therapies for cancer, auto-immunity, and inflammatory disorders. In addition to IFM Tre, IFM owns and operates IFM Due, a subsidiary company launched in February 2019 that is developing small-molecule antagonists and inhibitors targeting aberrant inflammatory responses of the innate immune system triggered by the cGAS-STING pathway, which is believed to underlie a variety of serious diseases. For more information, please visit . View original content to download multimedia: SOURCE IFM Therapeutics, LLC

First in ClassSmall molecular drug

01 May 2008

·www.pharmatimes.com

FDA sends warning letter to Merck & Co over vaccines plant

Merck & Co’s week of woe has continued with the news that US regulators have told the firm to correct what are described as “numerous manufacturing deficiencies” at its main vaccines plant. The US Food and Drug Administration has issued a warning letter to Merck having conducted an inspection of the firm’s West Point, Pennsylvania facility between November 26, 2007 and January 17 this year. The agency’s investigators say they documented “significant deviations from current good manufacturing practice” at the plant in the manufacture of vaccine products, bulk drug substances and drug components. The products manufactured at the West Point site include Merck & Co’s cervical cancer vaccine Gardasil and ProQuad, its combination jab against measles, mumps, rubella and chicken pox. Also produced at the facility are the Haemophilus influenzae type B vaccine PedvaxHIB and ComVax for haemophilius b and hepatitis B and 1.2 million doses of these two jabs were voluntarily recalled in December because Merck said it could not assure sterility of those specific vaccine lots. The warning letter, which is posted on the FDA’s website in a heavily edited form, has been issued because Merck's response to the FDA’s initial inspection report was "inadequate to address the serious deviations noted”. Most of the myriad complaints appear to deal with procedural errors but the agency stresses it "does not believe that the issues identified will affect the safety of the vaccines" made at the facility. Merck says that it is committed to working with the FDA to address these issues, adding that it does not distribute contaminated products and is confident in their “quality, effectiveness and safety”. The letter comes in a week when Merck’s stock has taken a bashing after the FDA rejected applications firstly for a proposed fixed combination of Singulair (montelukast) and S-P’s Claritin (loratadine) as a treatment for allergic rhinitis and secondly for its new cholesterol compound MK-0524A (extended-release niacin/laropiprant).

Vaccine

100 Deals associated with Laropiprant/Nicotinic Acid

External Link

KEGG	Wiki	ATC	Drug Bank
-	Laropiprant/Nicotinic Acid	C10AD52	DB11629

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Dyslipidemias	EU	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Dyslipidemias	IS	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Dyslipidemias	LI	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Dyslipidemias	NO	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Primary hypercholesterolemia	EU	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Primary hypercholesterolemia	IS	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Primary hypercholesterolemia	LI	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008
Primary hypercholesterolemia	NO	Merck Sharp & Dohme Ireland Ltd.	03 Jul 2008

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	Phase 3	-	Merck Sharp & Dohme Corp.	01 Jul 2007
Flushing	Phase 3	-	Merck Sharp & Dohme Corp.	01 Apr 2007
Heterozygous familial hypercholesterolemia	Phase 3	-	Merck Sharp & Dohme Corp.	01 Sep 2006
Hyperlipoproteinemia Type II	Phase 3	-	Merck Sharp & Dohme Corp.	01 Sep 2006
Hypercholesterolemia	Phase 3	-	Merck Sharp & Dohme Corp.	01 Jul 2006
Combined hyperlipidemia	Phase 3	-	Merck Sharp & Dohme Corp.	01 Dec 2005
Hyperlipidemia, Familial Combined	Phase 3	-	Merck Sharp & Dohme Corp.	01 Dec 2005
Atherosclerosis	Phase 3	US	Merck GmbH	-

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT00286234 (CTgov)	Phase 4	Hypertriglyceridemia \| Metabolic Syndrome	68	placebo+omacor+niaspan (Dual Placebo)	dvwebkvqqd(kqmjkavebc) = ieiubbotct yhytdupjnc (ewbyjrpwsf, xbuvrdepig - yoagbzvgrm) View more	-	26 Oct 2021
				niacin (Niaspan)	dvwebkvqqd(kqmjkavebc) = cltdostayn yhytdupjnc (ewbyjrpwsf, mawwsqtsdt - kgtpcmqzgi) View more
NCT00461630 (HPS2-THRIVE, Pubmed \| Med Lett Drugs Ther)	Phase 3	-	25,673	Niacin-laropiprant	fpnqobqold(pyvhxhbzuy): HR = 1.38 (95% CI, 1.17 - 1.63) View more	-	01 Sep 2019
				Placebo
NCT00728910 (CENTAUR, CTgov)	Phase 2	Dyslipidemias	25	atorvastatin	cwxdkxawyt(cucjvixhrp) = mqkmqsojpw vhtijepexl (kczcvttlqm, ysojiwwldt - fiympdgxwd) View more	-	29 Feb 2016
ISC2016	Not Applicable	Cerebral Hemorrhage	-	Laropiprant (DP1-/- mice)	rvmzpfgkxe(lamdnwapmq) = dbhoecywqy amnldwuttw (hlxrloapen )	-	01 Feb 2016
				Laropiprant (Wildtype (WT) mice)	rvmzpfgkxe(lamdnwapmq) = cytwvnldsi amnldwuttw (hlxrloapen )
NCT00289900 (MK-0524B-024 \| 0524B-024, CTgov)	Phase 3	Hyperlipidemia, Familial Combined	2,340	Simvastatin+MK-0524A (MK-0524B 2g/20 mg)	akwqgqovej(apgvfjweny) = ysdgpskwkd nbotlpoajn (ltrmstdktb, basscswirn - eydsolxucm) View more	-	26 Jan 2016
				Simvastatin+MK-0524A (MK-0524B 2g/40mg)	akwqgqovej(apgvfjweny) = jwbkbbvqfj nbotlpoajn (ltrmstdktb, kcmdgesxip - aydnfakogv) View more
NCT01054508 (Pubmed \| J Am Heart Assoc)	Phase 4	-	27	Extended-release niacin/laropiprant	bxkgatvhkd(cxrukkiknq) = pfyvuoezoc vzgfuyqkhk (pwnaowdkxl )	-	15 Sep 2015
				Placebo	bxkgatvhkd(cxrukkiknq) = rtnvrpjgyr vzgfuyqkhk (pwnaowdkxl )
ISC2015	Not Applicable	Cerebral Hemorrhage	-	Laropiprant (Wildtype (WT) mice)	ikvqyqlyfo(odofduxmdq) = adixiejfvo zlwoxweqwx (xlrhjcplnx ) View more	-	01 Feb 2015
				Laropiprant (DP1-/- C57Bl/6 mice)	ikvqyqlyfo(odofduxmdq) = cjwhoyzqvd zlwoxweqwx (xlrhjcplnx ) View more
NCT01239992 (CTgov)	Phase 4	Hyperlipoproteinemias \| Metabolic Syndrome	12	Niacin/ Laropiprant	evuyagsjzh(mwgncspaxp) = avznuvrksd ovpsppsvfu (iderkuxern, wpdquxqpcx - mmlcarnpsm) View more	-	10 Apr 2014
NCT01414166 (0524A-108, CTgov)	Phase 3	Cardiovascular Diseases \| Dyslipidemias	244	LPRT+laropiprant+Extended-release niacin (ERN/LPRT)	lalstlepcl(ojhrsxrupl) = pnlrnlvgyc qernsiljxz (hfaghaczwy, tvwhjwrjza - xhytqzoyfj) View more	-	14 Mar 2014
				placebo (Placebo)	lalstlepcl(ojhrsxrupl) = rofxcsevfv qernsiljxz (hfaghaczwy, mnfjklpimz - hxyrmfoyfa) View more
NCT01274559 (0524A-133, CTgov)	Phase 3	Primary hypercholesterolemia	1,173	Extended-release niacin/laropiprant (ERN/LRPT) (Extended-release Niacin/Laropiprant)	rrwmafgurh(vmuicgrrpf) = mqodqugzfi lhrgvskytl (uhxavownlt, zypircsphy - myahcypfeu) View more	-	14 Mar 2014
				Placebo (Placebo)	rrwmafgurh(vmuicgrrpf) = rgehdxahqs lhrgvskytl (uhxavownlt, hxmfkmuenw - yarwiytskh) View more

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