The main purpose of this study is to evaluate how much of the study drug (LY3372689), administered as a single dose that has the radioactive substance 14C incorporated into it, passes from blood into urine, feces and expired air in healthy male participants. The study will also measure how much of the study drug gets into the bloodstream, how its broken down, and how long it takes the body to get rid of it. The study will last about 4 weeks. Screening is required within 28 days prior to the start of the study and follow up is required approximately 7 days after discharge.

Start Date24 Feb 2023

Sponsor / Collaborator

Eli Lilly & Co.

NCT05063539 / Active, not recruitingPhase 2

Assessment of Safety, Tolerability, and Efficacy of LY3372689 in Early Symptomatic Alzheimer's Disease

The purpose of this study is to assess the safety, tolerability and effect of study drug LY3372689 in participants with early symptomatic Alzheimer's Disease

Start Date16 Sep 2021

Sponsor / Collaborator

Eli Lilly & Co.

NCT04392271 / CompletedPhase 1

Assessment of Brain O-GlcNAcase (OGA) Enzyme Occupancy After Multiple Oral Doses of LY3372689 as Measured by Positron Emission Tomography (PET) With the Radioligand [18F]LY3316612 in Healthy Subjects

This study uses imaging to evaluate how LY3372689 binds to a protein in the brain. This study will be conducted in healthy participants and will last up to about 10 weeks. Screening must be completed within four weeks prior to enrollment.

Start Date06 Aug 2020

Sponsor / Collaborator

Eli Lilly & Co.

100 Clinical Results associated with LY-3372689

100 Translational Medicine associated with LY-3372689

100 Patents (Medical) associated with LY-3372689

103

Literatures (Medical) associated with LY-3372689

30 Oct 2023·Reproduction (Cambridge, England)

Effect of vitrification on protein O-GlcNAcylation in mouse metaphase II oocytes

Article

Author: Gao, Feng ; He, Qifu ; Lan, Tianyang ; Liu, Ruichuan ; Wu, Shenghui ; Lin, Feifei ; Li, Hongmin ; Quan, Fusheng ; Zhang, Kang ; Kang, Jian

In brief:

Oocyte vitrification leads to DNA hypomethylation, which results in defect in early embryo development. This study reveals that oocyte vitrification impairs the DNA methylation pattern by influencing protein O-GlcNAcylation.

Abstract:

Oocyte vitrification leads to decreased DNA methylation levels, which impairs the quality and the developmental potential of oocytes. However, the underlying molecular mechanism still need to be further revealed. In this study, mouse metaphase II (M II) oocytes were frozen by vitrification technology, while fresh oocytes were used as the control group. The effect of oocyte vitrification on protein O-GlcNAcylation and its impact on the developmental potential of oocytes were elucidated. We found that the protein O-GlcNAcylation levels were significantly increased in vitrified oocytes. Increase of protein O-GlcNAcylation levels in control oocytes by PUGNAc (an O-GlcNAcase inhibitor) decreases blastocyst rate after parthenogenetic activation (20.82% in PUGNAc-treated group; 53.82% in control group, P < 0.05). We also discovered that DNA methylation was disrupted in two-cell embryos derived from vitrified oocytes, resulting in decreased 5mC and increased 5hmC, showing similar phenotypes to that derived from PUGNAc-treated oocytes. In vitrified and PUGNAc-treated oocytes, O-GlcNAcylated TET3 was significantly increased. Notably, by inhibiting protein O-GlcNAcylation in vitrified oocytes using OSMI1 (an O-GlcNAc transferase inhibitor) we restored the DNA methylation in two-cell embryos and ameliorated the developmental defects in early embryo. Thus, elevated protein O-GlcNAcylation in vitrified oocytes is an essential contributor to their declining embryonic developmental potential. Modulation of protein O-GlcNAcylation improves the developmental potential of vitrified oocytes.

02 Jun 2023·Cancer cell international

Synergistic apoptosis by combination of metformin and an O-GlcNAcylation inhibitor in colon cancer cells.

Article

Author: Choi, Soo Young ; Lee, Hae Min ; Lee, Geun Yong ; Lee, Su Jin ; Kwon, Oh-Shin ; Lee, Da Eun

BACKGROUND:

Although autophagy is an important mediator of metformin antitumor activity, the role of metformin in the crosstalk between autophagy and apoptosis remains unclear. The aim was to confirm the anticancer effect by inducing apoptosis by co-treatment with metformin and OSMI-1, an inhibitor of O-GlcNAcylation, in colon cancer cells.

METHODS:

Cell viability was measured by MTT in colon cancer cell lines HCT116 and SW620 cells. Co-treatment with metformin and OSMI-1 induced autophagy and apoptosis, which was analyzed using western blot, reverse transcription-polymerase chain reaction (RT-PCR) analysis, and fluorescence-activated cell sorting (FACS). Combined treatment with metformin and OSMI-1 synergistically inhibit the growth of HCT116 was confirmed by xenograft tumors.

RESULTS:

We showed that metformin inhibited mammalian target of rapamycin (mTOR) activity by inducing high levels of C/EBP homologous protein (CHOP) expression through endoplasmic reticulum (ER) stress and activating adenosine monophosphate-activated protein kinase (AMPK) to induce autophagy in HCT116 cells. Interestingly, metformin increased O-GlcNAcylation and glutamine:fructose-6-phosphate amidotransferase (GFAT) levels in HCT116 cells. Thus, metformin also blocks autophagy by enhancing O-GlcNAcylation, whereas OSMI-1 increases autophagy via ER stress. In contrast, combined metformin and OSMI-1 treatment resulted in continuous induction of autophagy and disruption of O-GlcNAcylation homeostasis, resulting in excessive autophagic flux, which synergistically induced apoptosis. Downregulation of Bcl2 promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and CHOP overexpression, synergistically inducing apoptosis. The activation of IRE1α/JNK signaling by OSMI-1 and PERK/CHOP signaling by metformin combined to inhibit Bcl2 activity, ultimately leading to the upregulation of cytochrome c release and activation of caspase-3.

CONCLUSIONS:

In conclusion, combinatorial treatment of HCT116 cells with metformin and OSMI-1 resulted in more synergistic apoptosis being induced by enhancement of signal activation through ER stress-induced signaling rather than the cell protective autophagy function. These results in HCT116 cells were also confirmed in xenograft models, suggesting that this combination strategy could be utilized for colon cancer treatment.

01 Nov 2022·British journal of anaesthesia

Hypoxia-triggered O-GlcNAcylation in the brain drives the glutamate–glutamine cycle and reduces sensitivity to sevoflurane in mice

Article

Author: Ou, Wei ; Zhou, Jian ; He, Qin-Qin ; Xie, Maodi ; Yu, Hai ; Lu, Peilin ; Wu, Wei ; Tang, Kuo ; Li, Tao ; Liang, Yu ; Huang, Jing ; Yang, Man ; Zuo, Yunxia ; Zhang, Yong

BACKGROUND:

Hypersensitivity to general anaesthetics predicts adverse postoperative outcomes in patients. Hypoxia exerts extensive pathophysiological effects on the brain; however, whether hypoxia influences sevoflurane sensitivity and its underlying mechanisms remain poorly understood.

METHODS:

Mice were acclimated to hypoxia (oxygen 10% for 8 h day^-1) for 28 days and anaesthetised with sevoflurane; the effective concentrations for 50% of the animals (EC₅₀) showing loss of righting reflex (LORR) and loss of tail-pinch withdrawal response (LTWR) were determined. Positron emission tomography-computed tomography, O-glycoproteomics, seahorse analysis, carbon-13 tracing, site-specific mutagenesis, and electrophysiological techniques were performed to explore the underlying mechanisms.

RESULTS:

Compared with the control group, the hypoxia-acclimated mice required higher concentrations of sevoflurane to present LORR and LTWR (EC50_LORR: 1.61 [0.03]% vs 1.46 [0.04]%, P<0.01; EC50_LTWR: 2.46 [0.14]% vs 2.22 [0.06]%, P<0.01). Hypoxia-induced reduction in sevoflurane sensitivity was correlated with elevation of protein O-linked N-acetylglucosamine (O-GlcNAc) modification in brain, especially in the thalamus, and could be abolished by 6-diazo-5-oxo-l-norleucine, a glutamine fructose-6-phosphate amidotransferase inhibitor, and mimicked by thiamet-G, a selective O-GlcNAcase inhibitor. Mechanistically, O-GlcNAcylation drives de novo synthesis of glutamine from glucose in astrocytes and promotes the glutamate-glutamine cycle, partially via glycolytic flux and activation of glutamine synthetase.

CONCLUSIONS:

Intermittent hypoxia exposure decreased mouse sensitivity to sevoflurane anaesthesia through enhanced O-GlcNAc-dependent modulation of the glutamate-glutamine cycle in the brain.

News (Medical) associated with LY-3372689

26 Mar 2024

·www.prnewswire.com

Asceneuron Joins Critical Path for Alzheimer's Disease Consortium

Consortium brings together industry, academic, and regulatory experts to advance research and bridge gaps in drug development targeting Alzheimer's disease Asceneuron to contribute its expertise in neurodegenerative disease to advance biomarkers for drug development in Alzheimer's disease LAUSANNE, Switzerland and SAN FRANCISCO, March 26, 2024 /PRNewswire/ -- Asceneuron SA, a clinical stage biotech company dedicated to targeting the root causes of neurodegenerative diseases, today announces that it has joined the Critical Path Institute's, Critical Path for Alzheimer's Disease (CPAD) Consortium. With its highly experienced leadership team and world class Scientific Advisory Board of leading experts in neurodegenerative diseases, Asceneuron is well positioned to contribute to the consortium. Asceneuron has an exemplary pipeline of O-GlcNAcase (OGA) inhibitors in clinical development that have the potential to halt disease progression in neurodegenerative diseases. Its lead asset, ASN51, is a potential best-in-class, orally administered, OGA inhibitor targeting tau aggregation and will be progressing into Phase II clinical development later this year. The CPAD consortium is proceeding to advance important biomarkers for Alzheimer's disease (AD), such as tau Positron Emission Tomography (PET) and is accelerating the pathway for approval of promising new therapies. As a member of CPAD, Asceneuron will work collaboratively with the consortium to help address the large unmet medical need of patients and families suffering due to neurodegenerative diseases. Ryan Schubert, Senior Vice President Research and Development at Asceneuron, said: "We are honored to be collaborating with the CPAD consortium alongside esteemed fellow members, all of whom are dedicated to accelerating drug development to improve patients' lives. CPAD has gathered high quality data and experts from industry, academia and regulatory agencies with a focus on bringing new treatment options to patients suffering with AD. We look forward to contributing to and impacting the treatment pathway for AD as we advance our lead intracellular tau-targeting asset, ASN51, into Phase II clinical development later this year. Further information will be shared at upcoming scientific conferences." Yashmin Karten, PhD, MBA, Associate Director at Critical Path for Alzheimer's Disease, added: "C-Path is proud to welcome Asceneuron as the newest member of its CPAD Consortium. Asceneuron's research on molecules that prevent the formation of toxic tau aggregates in the brain to slow down or stop the progression of AD provides a welcome addition to the intellectual brain power and wealth of scientific knowledge within the consortium. CPAD's diverse stakeholders and members are dedicated to enhancing regulatory decision-making tools to advance drug development and improve the lives of those living with AD and related dementia (ADRD). CPAD's mission is to accelerate the drug development process for patients with chronic neurodegenerative disease leading to dementia. Its primary focus is on AD. CPAD works with industry, regulatory authorities, academia, and patient advocacy organizations to aggregate anonymized patient-level data consensus standards with the aim of advancing drug development tools for evaluating drug efficacy and safety, to optimize novel clinical trial designs, and facilitating the regulatory review process." CPAD's integrated and standardized patient-level database comprises over 100,000 patient level records across 73 separate clinical trial datasets. These records are utilized by over 370 institutions worldwide. Alongside its biotech and pharmaceutical company members, the initiative incorporates feedback from all its stakeholders, including government and regulatory agencies. CPAD has ongoing efforts as part of its pre-competitive working groups to evaluate the potential of tau PET as a reliable surrogate endpoint, with the aim of enhancing efficiency in Alzheimer's disease drug development. About Asceneuron Asceneuron is a clinical stage biotech company focused on the development of orally bioavailable therapeutics for debilitating neurodegenerative disorders with high unmet medical need. The company's pipeline reflects its ambition and commitment to developing treatments for a wide a range of neurodegenerative diseases including Alzheimer's and Parkinson's disease, as well as orphan tauopathies. Asceneuron has two clinical-stage small molecule O-GlcNAcase inhibitors in development for the treatment of proteinopathies: OGA inhibitor ASN90 (licensed to Ferrer Pharmaceuticals) for the treatment of progressive supranuclear palsy (PSP) and a potential best-in-class OGA inhibitor, ASN51 for Alzheimer's disease. Asceneuron is backed by a renowned syndicate of investors consisting of Sofinnova Partners, M Ventures, SR One, Johnson & Johnson Innovation – JJDC, Inc. (JJDC) and Kurma Partners. For more information, please visit . About Critical Path Institute Critical Path Institute (C-Path) is an independent, nonprofit established in 2005 as a public-private partnership, in response to the FDA's Critical Path Initiative. C-Path's mission is to lead collaborations that advance better treatments for people worldwide. Globally recognized as a pioneer in accelerating drug development, C-Path has established numerous international consortia, programs and initiatives that currently include more than 1,600 scientists and representatives from government and regulatory agencies, academia, patient organizations, disease foundations and pharmaceutical and biotech companies. With dedicated team members located throughout the world, C-Path's global headquarters is located in Tucson, Arizona and C-Path's Europe subsidiary is headquartered in Amsterdam, Netherlands. For more information, visit . About Critical Path for Alzheimer's Disease (CPAD) Consortium Founded in 2008, the Critical Path for Alzheimer's Disease (CPAD) enhances regulatory decision-making tools to advance drug development and improve the lives of those living with Alzheimer's disease and related dementia (ADRD). The primary objective of Critical Path for Alzheimer's Disease (CPAD), a pre-competitive consortium of the Critical Path Institute, is to promote, support, and manage data and knowledge sharing from Alzheimer disease (AD) drug development stakeholders. CPAD generates the appropriate tools for the specific challenges identified by our stakeholders, to accelerate drug development for AD and advancing better treatments for people worldwide. For more information, please visit . SOURCE Asceneuron SA

Phase 2

07 Mar 2024

·www.fiercebiotech.com

Tau, anti-inflammation and orals form Biogen's future Alzheimer's pipeline

Biogen has two clinical-stage Alzheimer's disease assets behind Leqembi, both of which target tau proteins or their dysfunction. “What does it mean to be a leader in Alzheimer’s disease?” That’s the question Biogen is asking itself, and the question many of the company’s peers are working fervently to answer as the heated race to differentiate from the first batch of Alzheimer’s treatments turns to a simmer. Adam Keeney, Ph.D., corporate development chief for the Leqembi co-maker, said in an interview with Fierce Biotech that Biogen is "not only just satisfied with [amyloid] beta" and instead "looking at the different pillars of disease." Keeney says the first stop on the portfolio-building circuit is tau. The company’s phase 2 antisense drug, BIIB-080, targets the protein buildup that accompanies amyloid beta in patients with Alzheimer’s. It’s an intrathecal injection—an injection into the spinal cord to bypass the blood-brain barrier— which Keeney described as “not ideal” though probably satisfactory for a first-generation option. But Biogen is planning for and think-tanking easier methods, like IV delivery and even oral compounds. “We're thinking about degraders and molecular glues and different technologies that we can use,” Keeney said. Biogen already has one oral option in the clinic, the O-GlcNACase inhibitor BIIB-131, a small molecule that looks to block the enzyme research has tied to tau’s dysfunction in Alzheimer’s patients. Keeney described oral delivery as a goal that’s on a “longer time horizon” routing the work back to the original question: What does it mean to be a leader in the space? Biogen has experienced the ups and downs of Alzheimer's drug discovery more acutely than probably any company. Its well-documented Aduhelm failure came to a much-expected conclusion earlier this year, when Biogen wound down all work on the approved med. Not only was it made obsolete by Leqembi, but the therapy was a corporate representation of time wasted. Meanwhile, Eli Lilly pressed on from behind, raising up donanemab, which is expected to get an FDA ruling any day now. The amyloid beta battle may not ultimately be an automatic reflection of tomorrow’s tau contest, or other options that may be discovered. Deeper into Biogen’s research work, the company is tinkering with novel anti-inflammatory targets, Keeney says. Targeting rogue tau buildup has proven difficult, just like amyloid. Lilly cut a phase 2 large-molecule zagotenemab in October 2021 after it failed to hit phase 2 endpoints. This followed phase 1 data showing four cases of brain bleeding (ARIA-H) across three patients, representing 19% of treated patients. Kenney says it remains to be seen whether that’s a genuine signal tied to tau-busting treatments—but it's certainly been an issue with Leqembi and donanemab. “I think it's probably too early to say there's a signal or not in that,” he said. “We have no signal that is preventing us to move forward.” Beyond drug development, critical advancements are happening in the Alzheimer’s diagnostic sector, with companies working to improve the tests that could detect amyloid buildup. There’s been such improvement in this area that a working group convened by the Alzheimer’s Association and the National Institute on Aging recently revised its criteria for diagnosing Alzheimer’s to include blood-based biomarkers. Keeney says those tests may not immediately be a primary diagnosis, but a negative result could preclude someone from an additional PET scan. “So we're also investing and working with collaborators because there are blood-brain barrier biomarkers that are out there,” Keeney said, noting they aren’t yet 100% predictive. “We're helping also get the predictive validity improved.” Despite the blood-based tests needing refinement, authors of the new testing criteria made clear that the future is now, and some tests provide “excellent diagnostic performance.” “The field is now in a transition phase during which plasma biomarkers are being integrated with traditional CSF and PET biomarkers,” the guidance states.

Phase 2Phase 1

06 Mar 2024

·www.prnewswire.com

Asceneuron Expands Scientific Advisory Board with World Leading Experts in Neurodegenerative Diseases

Significant appointments of industry and academic experts to support Phase II development of ASN51 in Alzheimer's disease LAUSANNE, Switzerland and SAN FRANCISCO, March 6, 2024 /PRNewswire/ -- Asceneuron SA, a clinical stage biotech company dedicated to targeting the root causes of neurodegenerative diseases, today announces the appointments of neurodegenerative disease experts to its Scientific Advisory Board (SAB). These include Dr Samantha Budd Haeberlein, PhD, Henrik Zetterberg, MD, PhD, Rik Ossenkoppele, PhD, and Christopher van Dyck, MD. Asceneuron is advancing development of its lead asset ASN51 into Phase II clinical development targeting Alzheimer's disease. This compound is a potential best-in-class, orally administered, OGA inhibitor targeting tau aggregation. The Scientific Advisory Board members have vast experience in clinical trial design and biomarkers and will help support this promising program through Phase II clinical development. ASN51 has demonstrated its potential as a pathbreaker to halt disease progression in tau-mediated neurodegenerative diseases with its safe and well tolerated profile and sustained high central enzyme occupancy. In the field of Alzheimer's disease, ASN51 has the potential to change the treatment paradigm for patients when it commences a Phase II clinical trial in the second half of 2024. Ryan Schubert, Senior Vice President Research and Development at Asceneuron, said: "There is strong momentum in the Alzheimer's disease field, driven by recent progress and developments. This is an exciting stage for Asceneuron as tau is now clinically validated as a target. Our once daily, orally administered anti-tau O-GlcNAcase inhibitor, ASN51, has the potential to be best in class based on its unique pharmacology. I am honored to have these stellar neurodegenerative experts join our SAB at a fundamental time of development. Their deep knowledge and expertise will be invaluable as we move ASN51 into Phase II development." Dr Samantha Budd Haeberlein, PhD, is an esteemed figure in neurological drug development with international experience at research and executive levels in the discovery and development of therapeutics and biomarkers for neurodegenerative diseases. She was previously Senior Vice President and Head of Neurodegeneration at Biogen, where she led and co-led the development of two FDA approved treatments for Alzheimer's disease, ADUHELM and LEQEMBI. Samantha currently serves as the Chief Medical Officer at Enigma Biomedical Group, developing solutions for the treatment of neurodegenerative diseases, is on the Board of Directors at Vigil Neuro, and is a Senior Advisor to the ICG Life Sciences Investment team. Henrik Zetterberg, MD, PhD, is a decorated researcher in the field of neurodegenerative diseases. Henrik is a Professor of Neurochemistry at the University of Gothenburg, Sweden, and University College London (UCL), UK, and is a Clinical Chemist at Sahlgrenska University Hospital in Gothenburg, Sweden. He is Head of the Department of Psychiatry and Neurochemistry at the University of Gothenburg, leads the UK DRI Fluid Biomarker Laboratory at UCL, and is a Key Member of the Hong Kong Center for neurodegenerative diseases. He is also a Visiting Professor in the UW Department of Medicine, School of Medicine and Public Health, Madison, Wisconsin. Henrik has developed and researched new diagnostic tests and new preclinical models for Alzheimer's disease and has been recognised for his influential discoveries as a recipient of numerous prizes such as the Erik K. Fernström Prize for Junior Scientists and the Inga Sandeborg Prize for Research on Alzheimer's Disease. Rik Ossenkoppele, PhD, is a renowned academic in neuroscience, working at the intersection of neuroimaging, biomarkers, and cognition in Alzheimer's disease. Rik is an Associate Professor in Translational Neuroscience and is a Principal Investigator both at the Alzheimer center Amsterdam of the Amsterdam UMC and at Lund University in Sweden. Rik received the European Grand Prix for Research on the Foundation of Alzheimer's Disease in 2019, the Young Investigator Research award from Alzheimer Nederland in 2020, and the Queen Silvia Research prize in 2021. Christopher van Dyck, MD, is a leading clinical researcher focusing on neuroimaging and therapeutic studies of Alzheimer's disease and brain aging. He is a Professor of Psychiatry, Neurology, and Neuroscience and serves as Director of the Alzheimer's Disease Research Unit, the Alzheimer's Disease Research Center, and the Division of Aging and Geriatric Psychiatry at Yale School of Medicine. Alongside his academic positions, Christopher has extensive experience in leading and participating in more than 100 therapeutic trials in Alzheimer's disease, which include prodromal/ preclinical and brain aging stages. He serves on the Steering and Executive Committee and Co-Chairs the Protocol Evaluation Committee at the Alzheimer's Clinical Trials Consortium (ACTC). His extensive research has culminated in the lead authorship of the publication of the first disease-modifying treatment for AD (lecanemab) in 2023. About Asceneuron Asceneuron is a clinical stage biotech company focused on the development of orally bioavailable therapeutics for debilitating neurodegenerative disorders with high unmet medical need. The company's pipeline reflects its ambition and commitment to developing treatments for a wide a range of neurodegenerative diseases including Alzheimer's and Parkinson's disease, as well as orphan tauopathies. Asceneuron has two clinical-stage small molecule O-GlcNAcase inhibitors in development for the treatment of proteinopathies: OGA inhibitor ASN90 (licensed to Ferrer Pharmaceuticals) for the treatment of progressive supranuclear palsy (PSP) and a potential best-in-class OGA inhibitor, ASN51 for Alzheimer's disease. Asceneuron is backed by a renowned syndicate of investors consisting of Sofinnova Partners, M Ventures, SR One, Johnson & Johnson Innovation – JJDC, Inc. (JJDC) and Kurma Partners. For more information, please visit . SOURCE Asceneuron

Phase 2Executive Change

100 Deals associated with LY-3372689

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Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Phase 2	US	Eli Lilly & Co.	16 Sep 2021
Alzheimer Disease	Phase 2	JP	Eli Lilly & Co.	16 Sep 2021
Alzheimer Disease	Phase 2	AU	Eli Lilly & Co.	16 Sep 2021
Alzheimer Disease	Phase 2	CA	Eli Lilly & Co.	16 Sep 2021
Alzheimer Disease	Phase 2	PL	Eli Lilly & Co.	16 Sep 2021

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03819270 \| NCT04106206 (AAIC2021)	Not Applicable	-	-	LY3372689	fowsgbupiy(nnehkfrgpu) = LY3372689 was generally well tolerated up to the highest dose in each study, and no serious AE were reported. In the SAD, 40 treatment-emergent AEs (TEAEs) were reported, which were mostly mild in severity. The most common TEAEs were headache, nausea, pain in extremity, pain of skin, vessel puncture site pain, and limb discomfort. In the MAD, 42 TEAEs were reported, all of which were mild in severity. The most reported TEAE was headache. In both studies, there were no clinically significant changes in safety laboratories, including markers of inflammation, muscle injury, hormones and hepatoxicity. jymtodczgq (lfpwwcsywd )	-	31 Dec 2021
AAIC2021	Not Applicable	-	-	LY3372689 0.25 mg	wbggmifyql(cvalbfftkd) = curjjfoopt xqgfzvpmwl (temvfbmlco )	-	31 Dec 2021
AAIC2021	Not Applicable	-	-	LY3372689 1 mg	wbggmifyql(cvalbfftkd) = rhyeuuivzl xqgfzvpmwl (temvfbmlco )	-	31 Dec 2021
NCT03819270 (Literature) Manual	Phase 1	-	23	LY3372689	zctkwcxogy(kopcjbttib) = csplirsgqv klchnhmdse (nwfgcsygcs )	Positive	07 Dec 2020

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