The purpose of this study is to determine if there is any difference in the way the body handles 3 types of evacetrapib tablets with different particle sizes. Information about any side effects will also be collected. This study will consist of 3 study periods. Participants will be dosed 3 times during the entire study. Each study period will consist of an inpatient stay for 3 days - the day before dosing (Day -1), dosing day (Day 1) and the day after dosing (Day 2). Then participants will be asked to return to the clinical research unit (CRU) daily for outpatient appointments up to Day 8. The overall length of this study is about 7 weeks from first dose to end of study. Screening will take place within 28 days prior to the first dose of evacetrapib and follow-up will take place 21 days after the last dose of evacetrapib.

Start Date01 Jul 2015

Sponsor / Collaborator

Eli Lilly & Co.

NCT02260648

/ TerminatedPhase 3

A Double-Blind Efficacy and Safety Study of Evacetrapib in Combination With Atorvastatin in Japanese Patients With Primary Hypercholesterolemia

The main purpose of this study is to evaluate the efficacy and safety of the study drug known as evacetrapib when administered in combination with atorvastatin for 12 weeks in Japanese participants with primary hypercholesterolemia.

Start Date01 Jan 2015

Sponsor / Collaborator

Eli Lilly & Co.

NCT02365558

/ CompletedPhase 1

Evaluation of the Impact of Increased Gastric pH Following Omeprazole Administration on the Pharmacokinetics of Evacetrapib in Healthy Subjects

The purpose of this study is to evaluate the effect of increased stomach pH on how much evacetrapib is found in the blood stream and how long the body takes to get rid of it when given to healthy participants. Information about any side effects that may occur will also be collected.
There are two parts to the study. Participation in both parts will be required.
The study will last approximately 30 days, not including screening.

Start Date01 Jan 2015

Sponsor / Collaborator

Eli Lilly & Co.

100 Clinical Results associated with Evacetrapib

100 Translational Medicine associated with Evacetrapib

100 Patents (Medical) associated with Evacetrapib

Literatures (Medical) associated with Evacetrapib

24 Nov 2025·JCI Insight

High-throughput screens identify genotype-specific therapeutics for channelopathies

Article

Author: Do, Tri Q ; Shen, Alex ; Tellet Cabiya, Carlos ; Kroncke, Brett M ; Knollmann, Björn C ; Ku, Matthew ; Delisle, Brian P ; Egly, Christian L ; Woo, Suah ; Ritschel, Paxton A

Genetic diseases such as ion channelopathies substantially burden human health. Existing treatments are limited and not genotype specific. Here, we report a 2-step high-throughput approach to rapidly identify drug candidates for repurposing as genotype-specific therapy. We first screened 1,680 medicines using a thallium-flux trafficking assay against Kv11.1 gene variants causing long QT syndrome (LQTS), an ion channelopathy associated with fatal cardiac arrhythmia. We identified evacetrapib as a suitable drug candidate that improves membrane trafficking and activates channels. We then used deep mutational scanning to prospectively identify all Kv11.1 missense variants in an LQTS hotspot region responsive to treatment with evacetrapib. Combining high-throughput drug screens with deep mutational scanning establishes a paradigm for mutation-specific drug discovery translatable to personalized treatment of carriers with rare genetic disorders.

01 Jan 2025·DRUG RESISTANCE UPDATES

CEA-induced PI3K/AKT pathway activation through the binding of CEA to KRT1 contributes to oxaliplatin resistance in gastric cancer

Article

Author: Li, Weihua ; Tan, Song ; Yang, Changshun ; Mi, Yulong ; Hong, Weifeng ; Lin, Shengtao ; Liu, Shaolin ; Chen, Yifan ; Chen, Yizhen

BACKGROUND:

The serum level of carcinoembryonic antigen (CEA) has prognostic value in patients with gastric cancer (GC) receiving oxaliplatin-based chemotherapy. As the molecular functions of CEA are increasingly uncovered, its role in regulating oxaliplatin resistance in GC attracts attention.

METHODS:

The survival analysis adopted the KaplanMeier method. Effects of CEA on proliferative capacity were investigated using CCK8, colony formation, and xenograft assays. Oxaliplatin sensitivity was identified through IC₅₀ detection, apoptosis analysis, comet assay, organoid culture model, and xenograft assay. Multi-omics approaches were utilized to explore CEA's downstream effects. The binding of CEA to KRT1 was confirmed through proteomic analysis and Co-IP, GST pull-down, and immunofluorescence colocalization assays. Furthermore, small molecule inhibitors were identified using virtual screening and surface plasmon resonance.

RESULTS:

Starting from clinical data, we confirmed that CEA demonstrated superior ability to predict the prognosis of patients with GC who received oxaliplatin-based chemotherapy, particularly in predicting recurrence-free survival based on serum CEA level. In vitro and in vivo experiments revealed CEA^high GC cells presented increased proliferative capacity and decreased oxaliplatin sensitivity. The resistance phenotype was transmitted through secreted CEA. Multi-omics analysis revealed that CEA activated the PI3K/AKT pathway by binding to KRT1, leading to oxaliplatin resistance. Finally, the small molecule inhibitor evacetrapib, which competitively inhibits the CEA-KRT1 interaction, was identified and validated in vitro.

CONCLUSIONS:

In summary, the CEA-KRT1-PI3K/AKT axis regulates oxaliplatin sensitivity in GC cells. Treatment with small molecule inhibitors such as evacetrapib to inhibit this interaction constitutes a novel therapeutic strategy.

01 Sep 2024·Cell Reports Medicine

Uncovering therapeutic targets for macrophage-mediated T cell suppression and PD-L1 therapy sensitization

Article

Author: Coussens, Lisa M ; Malhotra, Sanjay V ; Schedin, Pepper ; Lee, Jee Min ; Malhotra, Sanjay V. ; Coussens, Lisa M. ; Keefe, Bailey F ; Nelson, Dylan ; Dheeraj, Arpit ; Tailor, Dhanir ; Kumar, Sushil ; Kummar, Shivaani ; Stefan, Kirsten ; Li, Wenqi ; Keefe, Bailey F.

Tumor-associated macrophages (TAMs) and other myelomonocytic cells are implicated in regulating responsiveness to immunotherapies, including immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis. We have developed an ex vivo high-throughput approach to discover modulators of macrophage-mediated T cell suppression, which can improve clinical outcomes of ICIs. We screened 1,430 Food and Drug Administration (FDA)-approved small-molecule drugs using a co-culture assay employing bone-marrow-derived macrophages (BMDMs) and splenic-derived T cells. This identified 57 compounds that disrupted macrophage-mediated T cell suppression. Seven compounds exerted prominent synergistic T cell expansion activity when combined with αPD-L1. These include four COX1/2 inhibitors and two myeloid cell signaling inhibitors. We demonstrate that the use of cyclooxygenase (COX)1/2 inhibitors in combination with αPD-L1 decreases tumor growth kinetics and enhances overall survival in triple-negative breast cancer (TNBC) tumor models in a CD8⁺ T cell-dependent manner. Altogether, we present a rationalized approach for identifying compounds that synergize with ICI to potentially enhance therapeutic outcomes for patients with solid tumors.

News (Medical) associated with Evacetrapib

17 Nov 2023

·synapse.patsnap.com

What are CETP inhibitors and how do you quickly get the latest development progress?

CETP, or Cholesteryl Ester Transfer Protein, plays a crucial role in lipid metabolism within the human body. It facilitates the transfer of cholesteryl esters (CE) and triglycerides (TG) between high-density lipoproteins (HDL) and low-density lipoproteins (LDL). By promoting the exchange of lipids, CETP contributes to the redistribution of cholesterol and triglycerides among lipoprotein particles. This process is essential for maintaining a healthy lipid profile and preventing the accumulation of cholesterol in the arteries. Understanding the function of CETP has led to the development of pharmaceutical interventions aimed at modulating its activity to improve cardiovascular health. Currently, the main drugs for increasing HDL-C include fibrates, niacin, and Cholesteryl Ester Transfer Protein (CETP) inhibitors. Among them, CETP inhibitors are the most potent in elevating HDL-C levels, making them a recent focus of major pharmaceutical companies. CETP is a plasma glycoprotein synthesized by the liver, most of which circulates in combination with HDL. The primary function of CETP is to mediate the transfer of cholesterol from HDL to VLDL and LDL during the process of triacylglycerol exchange, and CETP inhibitors can block this transfer process, theoretically possessing anti-atherosclerosis effects and the ability to reduce cardiovascular risks. The first CETP inhibitor developed by Pfizer in 2006, Torcetrapib, significantly increased HDL-C in coronary disease patients by 72.1%, but paradoxically, this increase led to a rise in cardiovascular events and mortality risk. In 2012, Dalcetrapib, a CETP inhibitor developed by Roche, significantly increased HDL-C levels by 31% to 40% compared to baseline in acute coronary syndrome patients during the dal-OUTCOMES phase III trial with an average follow-up of 31 months. However, the benefits in the primary endpoint (a composite of coronary death, nonfatal myocardial infarction, ischemic stroke, unstable angina, or cardiac arrest revival) were no better than the placebo group, and its development was also terminated. Lilly ceased development of its CETP inhibitor evacetrapib on October 12, 2015, and the prospects for Merck's anacetrapib are similarly bleak. However, research and development of CETP inhibitors have not stopped, with drugs such as BAY60-5521, JNJ-28545595, TA8895, and CKD519 gradually entering the preclinical development phase. Recent studies regarding the safety, tolerability, and pharmacodynamics of CKD-519 in a single ascending dose study with 40 healthy volunteers demonstrated that a single dose of CKD-519 (25 mg to 400 mg) significantly increased HDL-C levels without causing severe adverse events, nor causing an increase in blood pressure similar to that caused by Torcetrapib. Therefore, the issue that increasing HDL-C does not decrease cardiovascular events and mortality risk, as well as the future research direction for CETP inhibitors, have become recent points of discussion and research focus. How do they work?CETP inhibitors are a type of drug that target the cholesteryl ester transfer protein (CETP). CETP is a protein involved in the transfer of cholesterol esters between lipoproteins, such as high-density lipoprotein (HDL) and low-density lipoprotein (LDL). From a biomedical perspective, CETP inhibitors are designed to block the activity of CETP, thereby increasing the levels of HDL cholesterol and reducing the levels of LDL cholesterol. This mechanism is based on the understanding that higher levels of HDL cholesterol are associated with a lower risk of cardiovascular diseases, while elevated levels of LDL cholesterol are linked to an increased risk. By inhibiting CETP, these drugs aim to promote a favorable lipid profile and potentially reduce the risk of conditions like atherosclerosis, heart attacks, and strokes. However, it is important to note that the clinical efficacy and safety of CETP inhibitors are still being evaluated, and more research is needed to fully understand their potential benefits and risks. List of CETP InhibitorsThe currently marketed CETP inhibitors include: Ezetimibe/Pitavastatin CalciumDalcetrapibEvacetrapibObicetrapibObicetrapib/EzetimibeDRL-17822IcosabutateNST-1024CKD-508AnacetrapibFor more information, please click on the image below. What are CETP inhibitors used for?CETP inhibitors are approved indications include Hypercholesterolemia and Hyperlipoproteinemia Type II. For more information, please click on the image below to log in and search. How to obtain the latest development progress of CETP inhibitors?In the Synapse database, you can keep abreast of the latest research and development advances of CETP inhibitors anywhere and anytime, daily or weekly, through the "Set Alert" function. Click on the image below to embark on a brand new journey of drug discovery!

17 Sep 2023

·synapse.patsnap.com

Nemesis of Hypercholesterolemia - CETP inhibitors

CETP, or Cholesteryl Ester Transfer Protein, plays a crucial role in lipid metabolism within the human body. It facilitates the transfer of cholesteryl esters (CE) and triglycerides (TG) between high-density lipoproteins (HDL) and low-density lipoproteins (LDL). By promoting the exchange of lipids, CETP contributes to the redistribution of cholesterol and triglycerides among lipoprotein particles. This process is essential for maintaining a healthy lipid profile and preventing the accumulation of cholesterol in the arteries. Understanding the function of CETP has led to the development of pharmaceutical interventions aimed at modulating its activity to improve cardiovascular health. CETP Competitive LandscapeAccording to the data provided by Patsnap Synapse-Global Drug Intelligence Database: the following figure shows that as of 10 Sep 2023, there are a total of 39 CETP drugs worldwide, from 46 organizations, covering 25 indications, and conducting 173 clinical trials. 👇Please click on the picture link below for free registration or login directly if you have freemium accounts, you can browse the latest research progress on drugs , indications, organizations, clinical trials, clinical results, and drug patents related to this target. The analysis of target CETP from various perspectives provides valuable insights into the current competitive landscape and future development. Kowa Co., Ltd., NewAmsterdam Pharma Co. NV, and DalCor Pharmaceuticals Canada, Inc. are among the companies with drugs in advanced phases. Hypercholesterolemia and Hyperlipoproteinemia Type II are the approved indications for target CETP drugs. Small molecule drugs dominate the development landscape, with intense competition indicated by the presence of biosimilars. Japan, the United States, and the European Union are leading in terms of development, with China also making progress. Overall, the target CETP shows promising potential for addressing various indications related to cardiovascular diseases and lipid metabolism disorders. CETP Inhibitor Entering Phase III Clinical Trials:ObicetrapibObicetrapib is a small molecule drug that falls under the category of biomedicine. It specifically targets CETP. The drug is primarily focused on treating various therapeutic areas including Endocrinology and Metabolic Disease, Nervous System Diseases, and Cardiovascular Diseases. Obicetrapib has been identified to be effective in treating several active indications. These include Heterozygous familial hypercholesterolemia, Atherosclerosis, Dyslipidemias, Hypercholesterolemia, Alzheimer Disease, and Hyperlipidemias. These indications highlight the drug's potential in managing cholesterol-related disorders and neurodegenerative conditions such as Alzheimer's disease. 👇Please click on the image below to directly access the latest data (R&D Status | Core Patent | Clinical Trial | Approval status in Global countries) of this drug. The originator organization responsible for the development of Obicetrapib is Mitsubishi Tanabe Pharma Corp. This pharmaceutical company has been actively involved in the research and development of this drug. In terms of clinical development, Obicetrapib has reached Phase 3 of clinical development globally. This indicates that the drug has undergone extensive preclinical testing and has progressed to advanced stages of clinical trials involving a larger patient population. Phase 3 trials are crucial in evaluating the drug's safety, efficacy, and dosage requirements before seeking regulatory approval. Similarly, in China, Obicetrapib has also reached Phase 3 of clinical development. This suggests that the drug's development has progressed to an advanced stage in the Chinese market as well. In summary, Obicetrapib is a small molecule drug developed by Mitsubishi Tanabe Pharma Corp. It targets CETP and shows potential in treating various therapeutic areas such as Endocrinology and Metabolic Disease, Nervous System Diseases, and Cardiovascular Diseases. The drug has active indications including Heterozygous familial hypercholesterolemia, Atherosclerosis, Dyslipidemias, Hypercholesterolemia, Alzheimer Disease, and Hyperlipidemias. With its highest phase being Phase 3 globally and in China, Obicetrapib has undergone extensive clinical development and is currently being evaluated for its safety and efficacy in larger patient populations. EvacetrapibEvacetrapib is a small molecule drug that is being developed to target CETP (Cholesteryl Ester Transfer Protein). It falls under the therapeutic areas of endocrinology and metabolic disease, specifically focusing on the treatment of hypercholesterolemia, which is characterized by high levels of cholesterol in the blood. The drug is being developed by Eli Lilly & Co., a renowned pharmaceutical company. 👇Please click on the image below to directly access the latest data (R&D Status | Core Patent | Clinical Trial | Approval status in Global countries) of this drug. As of the latest available information, Evacetrapib has reached Phase 3 of clinical development, on a global scale. Phase 3 trials are conducted to evaluate the safety and efficacy of a drug in a larger population, typically involving thousands of patients. This indicates that Evacetrapib has successfully progressed through earlier stages of development, including preclinical studies and Phase 1 and 2 trials. However, it is important to note that the highest phase of development for Evacetrapib in China is listed as "discontinued." This suggests that the drug's development in China has been halted or terminated at some point, possibly due to various reasons such as lack of efficacy, safety concerns, or strategic decisions by the originator organization. In summary, Evacetrapib is a small molecule drug developed by Eli Lilly & Co. that targets CETP and is intended for the treatment of hypercholesterolemia. It has reached Phase 3 of clinical development globally, indicating promising progress in its development. However, in China, the drug's development has been discontinued, suggesting potential challenges or setbacks specific to the Chinese market.

25 Oct 2017

·www.biospace.com

Amgen Discontinues Quest for New CETP Heart Drug

Amgen inherited the drug after acquiring Dezima Pharma in a $1.2 billion deal in 2015. In 2015, P.K. Shah , director of atherosclerosis research at Cedars-Sinai Heart Center in Los Angeles, declared that CETP inhibitors were “dead” as legitimate drug targets. Shah said CETP inhibitors are a cardiologist’s dream that has not come true. Fast forward to today and it seems that Amgen may finally be in agreement with Shah’s statement. In its Third-quarterly report, Amgen announced it has scrapped internal development of AMG 899, an oral CETP inhibitor it acquired in the $1.2 billion deal for Netherlands-based Dezima Pharma BV. Amgen finally pulled the plug more than a year after it had suspended development of the CETP product. This morning, Amgen provided no details in its report as to what prompted the final decision to terminate the program, but that result further realizes Shah’s prediction. Amgen’s decision may have been linked to rival Merck ’s decision earlier this month to not submit regulatory filings for its cholesterol drug anacetrapib. In August, the company announced overall positive results for a four-year clinical trial of CETP drug anacetrapib. At the same time though, the company said the drug appeared to accumulate in fat tissue after extended dosing, which could hinder efficacy or create some unwanted adverse effects. At the time of Amgen’s 2015 acquisition of Dezima, analysts were already questioning if the cardiac drug was worth the cost. Two days after Amgen acquired AMG 899, Eli Lilly scrapped its Phase III CETP program that was testing if evacetrapib was a suitable treatment for high-risk atherosclerotic cardiovascular disease. Lilly pulled the plug on the CETP program following the recommendation of an independent data monitoring committee that said there was a “low probability” the study would achieve its primary endpoint based on results to date. CETP is a “cholesteryl ester transfer protein” which transfers cholesterol from HDL to VLDL Shah made the comment that CETP inhibitors were dead in an interview with Reuters following Lilly’s decision. Now with Amgen and Merck pulling out of the CETP development, it seems that the once-great hope for cholesterol treatment is, as Shah said, dead. Merck and Amgen are the two latest companies in a line who have shuttered their programming. In 2006, Pfizer terminated its trials for torcetrapib over safety concerns and in 2012, Roche discontinued studies of dalcetrapib for efficacy. Despite Roche’s failure, London-based DalCor is testing dalcetrapib in a subset of patients with a certain genotype, Endpoints News noted. Although AMG 899 is closed, Amgen still has other cholesterol treatments in its arsenal, such as Repatha, its PCSK9 drug. In its Q3 report, Amgen said Repatha sales increased “riven by higher unit demand.” And Repatha could continue to drive revenue. A Phase III study of Repatha on top of “maximally tolerated statin therapy in type 2 diabetic patients with hypercholesterolemia” met its co-primary endpoints of the percent reduction from baseline in LDL-C at week 12, and the mean percent reduction from baseline in LDL-C at weeks 10 and 12, with no new safety findings, Amgen reported. Amgen filed a supplemental Biologics License Application (sBLA) to include risk reduction of major cardiovascular events based on data from the large Repatha cardiovascular outcomes study. The U.S. Food and Drug Administration has set a Prescription Drug User Fee Act (PDUFA) target action date of Dec. 2, 2017.

Phase 3AcquisitionClinical ResultAHA

100 Deals associated with Evacetrapib

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KEGG	Wiki	ATC	Drug Bank
D10121	Evacetrapib	-	DB11655

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Primary hypercholesterolemia	Phase 3	Japan	Eli Lilly & Co.	01 Nov 2014
Hypercholesterolemia	Phase 3	United States	Eli Lilly & Co.	01 Oct 2014
Primary Hyperlipidemia	Phase 3	United States	Eli Lilly & Co.	01 Oct 2014
Acute Coronary Syndrome	Phase 3	United States	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	China	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	Japan	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	Argentina	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	Australia	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	Austria	Eli Lilly & Co.	01 Oct 2012
Acute Coronary Syndrome	Phase 3	Belgium	Eli Lilly & Co.	01 Oct 2012

Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01537887 (CTgov)	Phase 1	-	72	Placebo	mkyewchoey(ssujdguoxt) = ttuccjkfuo gnwypzfeyj (szgpmrogic, 7.5) View more	-	07 Mar 2019
NCT02271425 (CTgov)	Phase 1	-	8	Evacetrapib Tablet	kyqrbbqgtm(rpvuteilan) = opmzztqulk siyvjpyekb (baxqiuaahi, idcpayuran - wqxbvgxbhv) View more	-	01 Mar 2019
NCT02497391 (CTgov)	Phase 1	-	95	Evacetrapib (Evacetrapib Reference (R))	evqqxjfywu(qjoafijcxu) = ornxinvkon npuualycjj (opvyqqrlqm, 78) View more	-	03 Dec 2018
				Evacetrapib (Evacetrapib Test 1 (T1))	evqqxjfywu(qjoafijcxu) = wudnoyekkh npuualycjj (opvyqqrlqm, 56) View more
NCT01375075 (CTgov)	Phase 2	Dyslipidemias	165	Placebo+LY2484595 (100 mg LY2484595)	xjgpknmwln(pfbwlqngqo) = xukercggot ugakwdzfqj (pnubutxxss, 8.92) View more	-	25 Oct 2018
				Placebo+LY2484595 (500 mg LY2484595)	xjgpknmwln(pfbwlqngqo) = dfmggnvdzj ugakwdzfqj (pnubutxxss, 9.16) View more
NCT01836185 (CTgov)	Phase 1	Hepatic Insufficiency	32	Evacetrapib (Evacetrapib (Healthy))	gadodtlcsf(rcldlldsid) = amhckcguwp nrtqicsfwf (mfxqeibggy, 50) View more	-	12 Oct 2018
				Evacetrapib (Evacetrapib (Hepatic, Mild))	gadodtlcsf(rcldlldsid) = uwszaghhsq nrtqicsfwf (mfxqeibggy, 84) View more
NCT01810432 (CTgov)	Phase 1	-	40	Evacetrapib (Evacetrapib (Fasted))	ywczcfmhkb(pjrecsmqli) = cauutcbewn nywfcpxcse (zilpkonguh, 73) View more	-	12 Oct 2018
				High-fat Meal+Evacetrapib (Evacetrapib (Fed))	ywczcfmhkb(pjrecsmqli) = wvpezadiea nywfcpxcse (zilpkonguh, 22) View more
NCT02226653 (CTgov)	Phase 1	-	48	evacetrapib (Reference (Fasted))	qzlxwoxqok(krqywmskzg) = vpetgcoxzp orbqegeybj (jvxhpyqsxk, 40) View more	-	10 Oct 2018
				evacetrapib (Test (Fasted))	qzlxwoxqok(krqywmskzg) = qokskhwmgg orbqegeybj (jvxhpyqsxk, 36) View more
NCT01825889 (CTgov)	Phase 1	Cardiovascular Diseases	20	Evacetrapib (Evacetrapib (Participants With Renal Impairment))	rureuolruh(nggbotqiiy) = hrmtcsmvab syvupzadqf (uqgjmlummn, 49) View more	-	09 Oct 2018
				Evacetrapib (Evacetrapib (Healthy Participants))	rureuolruh(nggbotqiiy) = lalsavfnag syvupzadqf (uqgjmlummn, 37) View more
NCT01903434 (CTgov)	Phase 1	-	60	Evacetrapib (Reference)	cylsmenhbg(yhwalkcrqj) = korsvrgpbb oohjmpprnc (exsojdtjdn, 76) View more	-	09 Oct 2018
				Evacetrapib (Test)	cylsmenhbg(yhwalkcrqj) = yhveeabwve oohjmpprnc (exsojdtjdn, 102) View more
NCT01958489 (CTgov)	Phase 1	-	24	Pravastatin (Pravastatin (Period 1))	nozldvibcd(yycqtfqlrx) = xwijtnkfvi gmsugcrxry (rexyysuahs, 31) View more	-	09 Oct 2018
				Evacetrapib+Pravastatin (Evacetrapib + Pravastatin (Period 2))	nozldvibcd(yycqtfqlrx) = drphshcric gmsugcrxry (rexyysuahs, 43) View more

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