The study will evaluate the effect of oral contraceptive (birth control pill) on the blood level of lanabecestat when both are given together. Side effects will be monitored and documented. This study will last up to 27 days for each participant, not including screening. Screening is required within 42 days prior to first dose.

Start Date01 Jun 2018

Sponsor / Collaborator

Eli Lilly & Co.

[+1]

NCT03499041

/ WithdrawnPhase 1

Pharmacokinetics of LY3314814 in Subjects With Hepatic Impairment

The purpose of the study is to determine whether LY3314814 can be safely prescribed in participants with liver impairment without a dose adjustment. Participants will be on study for 11 days with follow-up about 7 days afterward.

Start Date01 Jun 2018

Sponsor / Collaborator

Eli Lilly & Co.

[+1]

NCT03545087

/ WithdrawnPhase 1

Pharmacokinetics of Lanabecestat (LY3314814) in Subjects With Impaired Renal Function

The purpose of the study is to determine whether lanabecestat can be safely prescribed in participants with kidney impairment without a dose adjustment.
Participants will be on study for up to 6 weeks; this includes a 2-week screening and a follow-up about 10 days after final drug administration.

Start Date01 Jun 2018

Sponsor / Collaborator

Eli Lilly & Co.

[+1]

100 Clinical Results associated with Lanabecestat

100 Translational Medicine associated with Lanabecestat

100 Patents (Medical) associated with Lanabecestat

Literatures (Medical) associated with Lanabecestat

01 Feb 2026·BIOORGANIC CHEMISTRY

Unraveling the metabolic potential of Moringa oleifera derived metabolites in combating Parkinson's and Alzheimer's disease

Article

Author: Nawaz, Muhammad Zohaib ; Sun, Xinxiao ; Alghamdi, Huda Ahmed ; Zhu, Daochen ; Haider, Syed Zeeshan ; Iqbal, Muhammad Waleed ; Yuan, Qipeng

Moringa oleifera is a nutrient-rich medicinal plant recognized for its broad-spectrum therapeutic potential. However, the specific bioactive metabolites and their molecular mechanisms in curing and preventing these diseases remain inadequately explored. The present study unveiled how moringa metabolites interact with specific molecular targets linked to various diseases and explored their potential as natural therapeutic agents against these diseases. The study first constructed a metabolite library based on compounds identified through multiple analytical techniques, including GC-MS, LC-MS, HPLC, UFLC, and NMR, as reported in previous studies. Then utilized a comprehensive computational approach integrating virtual screening, ADMET analysis, molecular docking, and dynamics simulations, and MM-GBSA/MM-PBSA methods to predict and evaluate the binding affinities and stabilities of moringa-derived metabolites against disease-related proteins. In total, 72 metabolites derived from moringa were screened against the ten genes, the overexpression of which was reported in five related disease conditions, including Alzheimer's, Parkinson's, Kidney Stones, Multiple Sclerosis, and Asthma diseases. These metabolites demonstrated strong interactions with genes associated specifically with Alzheimer's and Parkinson's diseases. To enhance the reliability and translational relevance of the computational predictions, experimentally validated inhibitors lanabecestat (APP inhibitor), GNE0877 (LRRK2 inhibitor), and olaparib (PARP1 inhibitor) were included as positive controls to benchmark the binding affinity and interaction stability of moringa metabolites. Our findings revealed that metabolites delta-tocopherol and gamma-tocopherol exhibit potential to inhibit poly (ADP-ribose) polymerase 1 (PARP1), while 1-acetyl-4,4-bis[4-(3-bromopropoxy)-3,5-dimethoxyphenyl] piperidine and 9,9'-bianthracene showed potential in inhibiting leucine-rich repeat kinase 2 (LRRK2); overexpression of both genes is linked to Parkinson's disease. Additionally, the metabolite 1-acetyl-4,4-bis[4-(3-bromopropoxy)-3,5-dimethoxyphenyl] piperidine also demonstrated potential in inhibiting the amyloid precursor protein (APP) associated with Alzheimer's disease. The identified metabolites displayed strong binding affinities, favorable ADMET properties, and stable interactions during molecular dynamics simulations compared to their respective control compound, positioning them as promising natural therapeutic agents against Alzheimer's and Parkinson's diseases. The study underscores the relevance of integrating computational methodologies to explore the therapeutic potential of bioactive plant compounds.

01 Dec 2025·BIOORGANIC CHEMISTRY

Design, synthesis, and biological evaluation of β-secretase inhibitors: An integrated study of molecular docking, dynamics, pharmacokinetics, quantum chemistry, and in-vitro analysis for Alzheimer's disease

Article

Author: Patel, Yamini ; Sharma, Pratibha ; Kumar, Ashok ; Parmar, Hamendra Singh ; Inwati, Gajendra Kumar

Present paper elicits the synthesis of a series of 2,2-dimethyl-2H-[1,3]dioxino[4,5-b]pyrrol-4(7H)-one derivatives as novel selective BACE1 inhibitors for the treatment of Alzheimer's disease (AD). A four-component, solvent-free condensation process, catalyzed by 10 mol% NiCl₂·6H₂O strategy was explored to achieve their synthesis. The structures of the synthesized compounds were ascertained using different spectroscopic techniques, including FT-IR, ¹H NMR, ¹³C NMR, mass spectrometry, and elemental analysis. In silico molecular docking and molecular dynamics simulations suggest that these compounds exhibit strong potential as β-secretase (BACE1) inhibitors, demonstrating high interaction and binding energies compared to reference inhibitors AZD3293 and E2602. Notably, compounds 5p displayed significant inhibitory interactions, effectively suppressing the catalytic dyad (Asp A:228 and Asp A:32) of BACE1. To further validate the computational findings, in vitro BACE1 enzymatic inhibition assays were performed on the most interactive molecule 5p. Additionally, ADMET descriptors and density functional theory (DFT) calculations were employed to assess the pharmacokinetics, chemical stability, and binding affinity of the synthesized compounds. The findings from this study pave the way for future in vivo investigations to assess the reversal of Alzheimer's disease phenotypes, along with comprehensive safety and toxicity evaluations.

01 Sep 2025·NEUROGASTROENTEROLOGY AND MOTILITY

Studying the Role of Myenteric Amyloidosis in Gastrointestinal Dysmotility and Enteric Neural Dysfunction Using APP/PS1 Mice—Is It an Adequate Animal Model?

Article

Author: Flood, Emma ; Srikrishna, Nikitha ; Galligan, James J. ; Xu, Hui ; Lansdell, Theresa A. ; Dorrance, Anne M. ; Fernandes, Roxanne ; Masino, Marlene ; Mui, Ryan

ABSTRACT:

Background:

The Gastrointestinal (GI) microbiome and gut‐brain axis are associated with the progression and pathology of Alzheimer's disease (AD). Amyloid deposition is thought to be a driver of AD, causing synaptic dysfunction and neuronal death in the brain. Chronic constipation is a common gastrointestinal (GI) dysmotility in AD patients, which impacts patient outcomes and quality of life. It is unknown if enteric amyloidosis disrupts myenteric neuron function and causes GI dysmotility.

Methods:

Untreated male and female APP/PS1 (a transgenic murine model of brain amyloidosis) and sex‐matched control mice were followed until 12 months of age. A separate cohort of mice was treated with a vehicle or the beta‐secretase (BACE1) inhibitor, lanabecestat, starting at 5 months of age until 7 months. GI motility was assessed in all mice by measuring whole GI transit in vivo. Propulsive colonic motility and GI smooth muscle contractions were measured ex vivo. At 7 or 12 months old, amyloidosis in the brain and myenteric plexus was determined by immunohistochemistry or ELISA; the myenteric neural density, including the cholinergic and nitrergic neurons, was evaluated by immune staining and RT‐PCR; expression of pro‐inflammatory factors in the GI wall was assessed by RT‐PCR.

Key Results:

By 7 months of age, male and female APP/PS1 mice developed abundant amyloid plaques in the brain. Aged untreated male APP/PS1 mice also demonstrated Aβ deposition in the colonic myenteric ganglia, which was associated with increased fecal output and faster whole GI transit starting at 4–7 months old, but vehicle‐ and lanabecestat‐treated male APP/PS1 mice had similar GI motility to their non‐genetic controls until 7 months old. None of the female APP/PS1 mice showed GI dysmotility or myenteric amyloidosis. Two months of lanabecestat treatment effectively reduced amyloid plaque burden in the brains of female APP/PS1 mice but not in male APP/PS1 mice. Treatment with lanabecestat did not affect myenteric Aβ intensity or GI motility in all APP/PS1 mice. All APP/PS1 mice did not show myenteric neuronal degeneration or inflammation until 12 months old.

Conclusions:

APP/PS1 mice do not recapitulate myenteric amyloidosis persistently and lack the phenotype of constipation observed in human AD patients; these mice should not be considered an adequate murine model for studying the role of myenteric amyloidosis in GI dysmotility. An adequate animal model with myenteric amyloidosis is required for further study.

News (Medical) associated with Lanabecestat

18 Jun 2018

·www.biospace.com

On “The Longest Day,” A Look at Alzheimer’s Clinical Trials

A shot of a senior man sitting on the sofa with his daughter, looking at a photograph. He is cuddling his daughter, looking sad and holding the photo. SolStock/Getty Images June is Alzheimer’s & Brain Awareness Month and June 21 is dubbed “The Longest Day,” which focuses on raising awareness of Alzheimer’s disease. June is Alzheimer’s & Brain Awareness Month and June 21 is dubbed “The Longest Day,” which focuses on raising awarenes s of Alzheimer’s disease. As most everyone knows, Alzheimer’s is a common form of dementia. In the U.S., it affects about 5.7 million people. Without any cure, it is estimated that by 2050, 14 million Americans will be living with the disease. The U.S. is expected to spend $277 billion on Alzheimer’s or other dementia care this year alone. Baby boomers, if a treatment isn’t developed, will push that number to $1.1 trillion by 2050. Unfortunately, so far, drug development for Alzheimer’s disease has been a barren wasteland of failed clinical trials. By at least one report, more than 190 Alzheimer drugs have failed in clinical trials. Recent failures include vTv Therapeutics ’ Phase III trial for azeliragon, which failed to meet primary endpoints; AstraZeneca and Eli Lilly ’s lanabecestat, which was abandoned this month; Johnson & Johnson ’s Janssen division ended its trials of atabacestat in May; and in February, Merck & Co . announced it was halting protocol 019, its APECS Phase III clinical trial of verubecestat (MK-8931). In a statement in June, Eli Lilly’s president of Lilly Research Labs, Daniel Skovronsky, said in a statement, “The complexity of Alzheimer’s disease poses one of the most difficult medical challenges of our time, and we are deeply disappointed for the millions suffering from this devastating disease.” In late January, Pfizer announced it was abandoning its research and development of new neuroscience programs and cutting eight different projects, of which four early-stage programs were for Alzheimer’s. But in June, the company threw another $600 million into its venture capital fund, with a quarter earmarked for neuroscience research investments. Although it seems grim, hopefully, it will turn out to be like Thomas Edison’s adage about inventing the light bulb, which was, “I have not failed. I’ve just found 10,000 ways that won’t work.” With any luck, biopharma won’t require 10,000 failures. With that in mind, here’s a look at some of the ongoing Phase III clinical trials in Alzheimer’s disease. The Alzheimer’s Association keeps tabs on ongoing trials, breaking them down to treatment trials, diagnostic studies, prevention trials, quality of life studies, and online studies. Those studies are broken down further into phases. In April, the association listed 15 ongoing Phase III trials for Alzheimer’s, with about another 27 for related symptoms. Unfortunately, some listed include those already terminated. However, here’s a look at some of the ongoing Phase III trials for Alzheimer’s disease. Biogen ’s aducanumab. Aducanumab is one of the top prospects for Alzheimer’s disease, although not without its skeptics. It is currently in a Phase III trial. The company sent tremors through its stock value in February when the company’s chief medical officer, Al Sandrock, speaking at the Leerink Healthcare Conference, said Biogen had added 510 more patients to the trial because, he said, “We did see more variability on the primary endpoint than assumed when we did the initial sample size estimations. So we decided to increase the sample size to maintain 90 percent power.” A lot of investors viewed that as the company said it wasn’t getting the results it expected, so was increasing its sample size. Originally some data was going to be presented at the end of the year, but it seems more likely in 2020, with possibly some interim data being released here and there before then. Aducanumab is an antibody that targets beta-amyloid, the plaques that build up in the brains of Alzheimer’s patients and is the primary theory behind the damage caused to cognition. Novartis and Amgen’s CAD-106 and CNP520. In September 2015, Novartis and Amgen entered into a global collaboration to commercialize and develop neuroscience treatments. One was a BACE inhibitor program for Alzheimer’s disease. BACE is involved in the development of beta-amyloid. CAD106 is designed as a vaccine against beta-amyloid. It is composed of a short piece of beta-amyloid that includes only the amino acids 1 to 6. The idea is it will trigger an immune response to prevent new plaques from forming. The study also is looking at CNP520 from Amgen. CNP520 is a BASE inhibitor. The study launched in October 2015 and is expected to run until at least 2020, and probably to 2023. Roche/Genentech’s crenezumab. Genentech announced in February 2017 that it was launching a second Phase III trial of crenezumab with its partner AC Immune . The CREAD2 trial will recruit 750 patients with prodromal or mild Alzheimer’s. Crenezumab is also an antibody against beta-amyloid. In a statement at the time, Andrea Pfeifer, the chief executive officer of AC Immune, said, “Given the recent disappointing results of other therapies, all of us in the Alzheimer’s community need to redouble our efforts to combat one of society’s biggest challenges. We remain confident about the potential of crenezumab given it is distinct from other beta amyloid antibodies, predominantly blocking oligomers in the brain, and has a clinical development program that is using higher dosing and targeting earlier stages of Alzheimer’s disease.” Biogen and Eisai’s elenbecestat. On June 4, the two companies announce d that in a Phase II clinical trial, the BACE inhibitor was found to be generally safe and well tolerated. It also showed a statistically significant difference in amyloid beta levels in the brain of patients as measured by amyloid-PET scans. There was also a possible delay of clinical symptoms. The trial involved 70 patients with mild cognitive impairment due to Alzheimer’s or mild to moderate dementia due to Alzheimer’s with confirmed amyloid pathology by PET scans. They were randomized to four treatment arms of elebecestat, 5, 15, or 50 mg, or placebo. The two companies are currently running two global Phase III clinical trials of the drug in early Alzheimer’s disease. “It is highly encouraging that Study 202 confirmed elenbecestat’s treatment effect in reducing amyloid in the brain and suggested a slowing of clinical decline,” said Lynn Kramer, chief clinical officer and chief medical officer, Neurology Business Group, Eisai, in a statement. “Eisai and Biogen will continue to work together to advance the ongoing Phase III program (MISSION AD) in order to contribute a new potential treatment option to Alzheimer’s disease patients as soon as possible.” Although there is no guarantee any of these trials will be the trial that breaks through with a new Alzheimer’s drug approval, many companies are continuing to learn more and more about the disease and test new approaches to treatment and prevention.

Phase 2Phase 3Clinical ResultVaccine

12 Jun 2018

·www.biospace.com

Eli Lilly and AstraZeneca Abandon Alzheimer’s Drug

Yet another drug for Alzheimer’s has been tossed in the trash. AstraZeneca and Eli Lilly announced they have abandoned two late-stage clinical trials of lanabecestat for Alzheimer’s disease. Yet another drug for Alzheimer’s has been tossed in the trash. AstraZeneca and Eli Lilly announced they have abandoned two late-stage clinical trials of lanabecestat for Alzheimer’s disease. The decision was made after an independent monitoring committee evaluated the results to date and concluded that its primary endpoints were “not likely” to be met. There were no safety concerns. The two companies say they will continue to work together on a different early-stage drug for Alzheimer’s. Lilly also has other Alzheimer’s drug in ongoing clinical trials. Lanabecestat is in a class of Alzheimer’s drugs called beta secretase cleaving enzyme (BACE) inhibitors. BACE is a precursor to amyloid-beta, which is believed to be the leading cause of Alzheimer’s disease. However, a number of recent high-pro of antibodies that clear amyloid-beta has cast doubt on the amyloid hypothesis. Later in the disease, tau proteins accumulate in the brains of Alzheimer’s patients, but that has not been as intense a focus as amyloid clearance or prevention. In February, Merck & Co. announced it was halting protocol 019, its APECS Phase III clinical trial of verubecestat (MK-8931) in Alzheimer’s disease. Verubecestat was also a BACE inhibitor. In that case, an external Data Monitoring Committee (eDMC) recommended ending the trial after an interim safety analysis indicated the likelihood of benefits didn’t outweigh the risks. In May, Johnson & Johnson ’s Janssen division ended its trials of atabacestat, a BACE inhibitor. It indicated, similar to Merck, that it was shuttering the program because of safety issues, rather than any question about the drug’s efficacy. Patients in the EARLY Phase IIb/III clinical trial with preclinical Alzheimer’s disease, as well as a Phase II long-term safety trial, had elevated liver enzymes. Lilly and AstraZeneca teamed up to co-develop lanabecestat in 2014 in a deal that could have hit $500 million. Lilly handled the two trials, one for early Alzheimer’s and the other for patients with a milder version of the disease. AMARANTH was for early Alzheimer’s and DAYBREAK-ALZ was on mild Alzheimer’s disease dementia. AstraZeneca handled manufacturing. The trials were expected to conclude in 2021. There were more than 3,000 patients enrolled. The drug received Fast Track designation in 2016 from the U . S. Food and Drug Administration (FDA) . “The complexity of Alzheimer’s disease poses one of the most difficult medical challenges of our time, and we are deeply disappointed for the millions suffering from this devastating disease,” said Daniel Skovronsky, president of Lilly Research Labs, in a statement. He went on to say, “We won’t give up on finding a solution for Alzheimer’s patients.” On the good-news-so-far front, it was only last week that Biogen and Eisai Co. announced that their BASE inhibitor, elenbecestat, had a good safety pro a Phase II clinical trial and showed a statistically significant difference in amyloid beta levels in the brain. Those levels were measured by amyloid-PET scans. That trial was of 70 patients and as the company noted, is the first trial of a BACE inhibitor to show a statistically significant difference in amyloid beta in the brain while also showing a delay of clinical symptom decline. “It is highly encouraging that Study 202 confirmed elenbecestat’s treatment effect in reducing amyloid in the brain and suggested a slowing of clinical decline,” said Lynn Kramer, Eisai’s chief clinical officer and chief medical officer, Neurology Business Group, in a statement. “Eisai and Biogen will continue to work together to advance the ongoing Phase III program (MISSION AD) in order to contribute a new potential treatment option to Alzheimer’s disease patients as soon as possible.”

Phase 2Fast TrackPhase 3Clinical Result

25 Jan 2018

·www.biospace.com

At Last: Eli Lilly Publishes Data for Catastrophic Alzheimer’s Trial

Lilly finally revealed the data in the New England Journal of Medicine. Has the amyloid plaque question in Alzheimer’s research been put to rest? Eli Lilly ’s recent data analysis of its failed Phase III Alzheimer’s disease treatment solanezumab would suggest so. In an article in the New England Journal of Medicine, Eli Lilly said solanezumab did not significantly slow cognitive decline in in Alzheimer’s patients. In 2016, Lilly reported the failure of solanezumab . But the company maintained hope that sola could be salvaged as a treatment for patients in the earliest stages of Alzheimer’s disease. Company researchers believed solanezumab would be effective at targeting amyloid- beta plaque and stop or at least significantly slow progression of the disease. But now that appears to be a dead end. In the NEJM article, Lilly said it failed to reach significance in determining if solanezumab was effective. The company said it enrolled 2,129 patients and provided 1,057 with solanezumab and the remaining 1,072 patients received a placebo. Lilly reported that the mean change from baseline in the ADAS-cog14 score was 6.65 in the solanezumab group and 7.44 in the placebo group, with no significant between-group difference at week 80. “Solanezumab at a dose of 400 mg administered every 4 weeks in patients with mild Alzheimer’s disease did not significantly affect cognitive decline,” Lilly said in the article abstract . Writing in Forbes, Arlene Weintraub said Lilly’s information will be “ sure to disappoint researchers who have been hanging onto the ‘amyloid hypothesis’ of Alzheimer’s.” Citing Michael Murphy , a professor at the University of Kentucky ’s Sanders-Brown Center on Aging Weintraub said Lilly’s failure should “raise questions” about the hypothesis. “Some success in preclinical studies evolved into this idea that what we need to do is remove the soluble form of the [amyloid-beta] peptide from the brain. But all [human] trials ended up being disappointing—they didn’t really work,” Murphy told Weintraub. Murphy didn’t close the door completely on whether or not the hypothesis was dead and noted that some continued studies, including Biogen’s aducanumab, should be watched closely. Biogen seems confident in the drug. In October, the Boston-based company announced it had increased its profit potential on the drug by forking over an additional $150 million to Neurimmune Holding AG , the company from which Biogen licensed the drug. That would reduce any future royalty payments Biogen would have to make should the AD drug prove marketable. Biogen released early data from its Phase Ib clinical trial of aducanumab, which revealed that patients receiving the drug showed a drop in Alzheimer’s-related beta-amyloid plaque in the brain, as well as continued to show a slowing of cognitive declines. Lilly also continues to see promise in the amyloid hypothesis. In an email to Weintraub, Lilly confirmed its commitment to developing a treatment for Alzheimer’s disease, which includes programs that target both amyloid-beta and tau tangles. “Because we now know that amyloid builds up in the brain 15-20 years before symptoms, the broader scientific community has hypothesized that Alzheimer’s may need to be targeted earlier in the disease progression. With the technology of new advanced diagnostics, many of the current studies target patients much earlier than ever before,” Lilly said in its email. Eli Lilly remains committed to developing a treatment for Alzheimer’s disease and has eight different experimental drugs in its pipeline, including lanabecestat, a BACE drug it licensed from AstraZeneca , as well as the failed sola. Lilly has a Phase I and Phase II BACE program. Alzheimer’s and other forms of dementia are a growing healthcare concern. In the United States, Alzheimer’s disease is the sixth-leading cause of death across all ages and the fifth-leading cause of death in people over 65 years of age. By 2050, the number of global patients is expected to hit 131.5 million.

Phase 1Phase 2Clinical ResultPhase 3

100 Deals associated with Lanabecestat

External Link

KEGG	Wiki	ATC	Drug Bank
D10946	Lanabecestat	-	DB14814

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Phase 3	Taiwan Province	AstraZeneca PLC	01 Jul 2016
Thrombosis	Phase 1	United States	AstraZeneca PLC	30 Sep 2015

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT02245737 (AMARANTH, CTgov)	Phase 2/3	Alzheimer Disease	2,218	Placebo (Placebo)	crffcssmvj(lkjaoanjfv) = detgsuihci tvgsqxkaxo (drapfhqyaf, 0.55) View more	-	06 Aug 2019
				Lanabecestat (Lanabecestat 50 mg)	crffcssmvj(lkjaoanjfv) = mqgszhjwgb tvgsqxkaxo (drapfhqyaf, 0.58) View more
NCT02783573 (DAYBREAK-ALZ, CTgov)	Phase 3	Alzheimer Disease	1,722	Lanabecestat	zjwzrpfydz(bmuwudpksr) = tmperxxyru ycxkbkfvqy (uocqhzhvgp, 1.32) View more	-	06 Aug 2019
NCT02972658 (CTgov)	Phase 3	Alzheimer Disease	421	Lanabecestat (AZES Placebo/AZFD Lanabecestat 20 mg)	jyamlriymp(vzwodskiga) = bkdcijypaw ulqntvncaj (clyeplyoey, 1.60) View more	-	05 Jul 2019
				Lanabecestat (AZES Placebo/AZFD Lanabecestat 50 mg)	jyamlriymp(vzwodskiga) = ulwethwnzl ulqntvncaj (clyeplyoey, 1.65) View more
NCT03019549 (CTgov)	Phase 1	-	42	Rosuvastatin	uzwrxxvddo(aegmhgploa) = uaxaxrnsxm vkyaqqytrm (mejlhgsyql, 47)	-	16 Apr 2019
NCT02568397 (CTgov)	Phase 1	-	60	Dabigatran etexilate	ehfquaajoo(zaafgxhmus) = jbvelmrgnj kaywzerefu (pnosplcbrg, 69) View more	-	05 Apr 2019
NCT02540668 (CTgov)	Phase 1	Thrombosis	15	Warfarin	vtvhpemlgp(zupyaeymog) = fyaudybylm znzxylzqwu (eypwoiybpj, 12) View more	-	25 Mar 2019
NCT02406261 (CTgov)	Phase 1	-	82	simvastatin+Midazolam+Lanabecestat (Cohort A)	rivwfwzffs(gfftxakfmm) = ludrlplaiu crqfnnovzl (iindiosmua, 21) View more	-	22 Mar 2019
				Lanabecestat+Donepezil (Cohort B)	tgaoyyjfyx(qhjdccxymx) = sogxqfphoz gcwascrlzc (mtfctqasac, 28) View more
NCT03222427 (CTgov)	Phase 1	-	8	LY3314814 (LY3314814)	solllebtew(rlleemwzdf) = vcvqxruogb rcdanyffdb (kbmcupthxh, 41) View more	-	22 Mar 2019
				[13C415N3] LY3314814 ([13C415N3] LY3314814)	solllebtew(rlleemwzdf) = ojbhsubcti rcdanyffdb (kbmcupthxh, 17) View more
NCT02663128 (CTgov)	Phase 1	-	18	LY3314814 (AZD3293) (R (Fasted))	qywplencyr(vscfqzbmcd) = spzinnubrc ptuccgihje (sfzraoovdo, 22) View more	-	22 Mar 2019
				LY3314814 (AZD3293) (T (Fasted))	qywplencyr(vscfqzbmcd) = ftncnsvysm ptuccgihje (sfzraoovdo, 22) View more

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