A Phase I, Randomized, Double-Blind, Placebo-Controlled, Single and Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of the Combination of Nilotinib, Marimastat, and Varespladib in Healthy Adult Volunteers - NIL

Start Date27 Jul 2026

Sponsor / Collaborator

Dycine Pharmaceuticals Limited

NCT05717062

/ CompletedPhase 2

Randomized, Double-Blinded, Placebo-Controlled Study to Evaluate the Safety, Tolerability, and Efficacy of Intravenous Varespladib Followed by Oral Varespladib in Addition to Standard of Care in Subjects Bitten by Venomous Snakes

This is a multicenter,randomized,double-blind, placebo-controlled, phase 2 study designed to evaluate the safety, tolerability and efficacy of a continuous rate infusion (CRI) of IV varespladib followed by transition to the oral dosage form, varespladib-methyl, concurrently with SOC, in participants bitten by venomous snakes.
Note: Funding Source - FDA-OOPD

Start Date30 May 2023

Sponsor / Collaborator

Ophirex, Inc.

CTRI/2021/11/037901

/ CompletedPhase 2

Randomized, Double-Blinded, Placebo-Controlled Add-On Therapy Study to Evaluate the Safety, Tolerability, and Efficacy of a Multi-Dose Regimen of Oral Varespladib-Methyl in Subjects Bitten by Venomous Snakes - BRAVO

Start Date01 Feb 2022

Sponsor / Collaborator

Ophirex, Inc.

100 Clinical Results associated with Varespladib

100 Translational Medicine associated with Varespladib

100 Patents (Medical) associated with Varespladib

135

Literatures (Medical) associated with Varespladib

01 Oct 2026·TOXICON

Comparison of the efficacy of varespladib and coral snake antivenom against the activities of the Amazon coral snake (Micrurus spixii) venom

Article

Author: da Rocha, Marisa M T ; Serino-Silva, Caroline ; Cantuaria, Nathalia M ; Passos, Fernanda R ; Prezoto, Benedito Carlos ; Oshima-Franco, Yoko ; Floriano, Rafael S ; Gutiérrez, José María ; Lewin, Matthew ; Hyslop, Stephen

The ability of varespladib (VPL), a phospholipase A₂ (PLA₂) inhibitor, to attenuate several activities of the Amazon coral snake (Micrurus spixii) venom was assessed. The neutralization by VPL was compared to that of coral snake antivenom and, in some cases, neostigmine. The venom showed anticoagulant activity in human plasma (assessed using in vitro thromboelastometry), and was myotoxic (based on the increase in serum creatine kinase activity) and lethal to mice, in addition to causing neuromuscular blockade in chick isolated biventer cervicis preparations. Antivenom fully protected against lethality but only partially neutralized the other activities at the doses tested. VPL attenuated PLA₂-dependent effects, including anticoagulant activity and myotoxicity, but did not abrogate lethality. A combination of VPL and antivenom was also effective against anticoagulant activity and myotoxicity. Antivenom and VPL were partially effective for inhibiting the neuromuscular blockade induced by the venom, suggesting that toxins other than PLA₂s might be also involved. Antivenom and Varespladib combined have a higher inhibition than each of them alone against anticoagulant, myotoxic and neuromuscular blocking effects. Neostigmine, an anticholinesterase drug, showed only modest protection against lethality and neuromuscular blockade. These findings suggest that VPL could be a potential adjunct to conventional antivenom therapy in treating envenomation by M. spixii.

02 Jul 2026·MOLECULAR CANCER THERAPEUTICS

Chromobox 2 Inhibition: A Novel Activity of Alisertib, an Aurora A Kinase Inhibitor

Article

Author: Nurmemmedov, Elmar ; Bitler, Benjamin G. ; Elder, Alan M. ; Petkov, Alexander ; Reigan, Philip ; Woodruff, Elizabeth R. ; Brubaker, Lindsay W. ; Eisenmesser, Elan ; Yamamoto, Tomomi M. ; Iwanaga, Ritsuko

Abstract:

Chromobox 2 (CBX2), a subunit of polycomb repressor complex 1 (PRC1), is expressed in high-grade serous carcinoma (HGSC). CBX2-inhibitory peptide (CBX2i) has demonstrated efficacy in a syngeneic mouse model but has limitations. We sought to identify an alternative approach to CBX2 inhibition. A computational-based molecular docking screen was performed using the Selleckchem Bioactive Library to identify inhibitors of CBX2. A similarity screen of top hits against the bound conformation of CBX2i pharmacophore model was performed in parallel. A series of in vitro validation studies evaluated the effect of alisertib on proliferation, a CBX2 target gene, and stemness. CBX2-knockdown cell lines and a syngeneic murine model were utilized to evaluate alisertib response in the context of CBX2 loss. Cell target engagement assay was performed. PRC1 activity was measured by H2AK119ub levels. Immune profiling of treated tumors defined the immune microenvironment. The computational-based screen identified 10 candidate compounds. In vitro validation narrowed compounds of interest to raltitrexed, alisertib, GTX-007, LY315920, and PD0325901. Ultralow dilution assay demonstrated a dramatic decrease in spheroid formation with alisertib, an aurora A kinase (AURKA) inhibitor. Good structural overlap was observed between CBX2i and alisertib. Cell target engagement assay confirmed alisertib selectivity for both AURKA and CBX2. Loss of CBX2 attenuated alisertib efficacy in vitro and in vivo. Treatment with alisertib leads to a decrease in H2AK119ub and shift in the immune tumor microenvironment. Alisertib efficacy in HGSC is dependent on functional CBX2, and cell target engagement confirms selectivity for CBX2, supporting that alisertib activity involves CBX2 inhibition.

01 Jul 2026·JOURNAL OF LIPID RESEARCH

Hydrolysis and depletion of phosphatidylglycerol at peak murine acute lung injury

Article

Author: Perez-Gil, Jesus ; Seeds, Michael C ; Olmeda, Barbara ; Novotny, Michael V ; Lloyd, Christopher M ; Satusky, Matthew J ; Hite, R Duncan ; Baer, Brandon

Anionic phospholipids are essential for surfactant function and phosphatidylglycerol (PG) is the most abundant. Increased secretory phospholipase A2 (sPLA₂) and disproportionate depletion of PG is consistently observed in patients with acute respiratory distress syndrome (ARDS), leading to speculation on their potential relationship. We hypothesized that a non-lethal murine model of acute lung injury (ALI) would demonstrate a temporal association between lung inflammation, surfactant dysfunction, PG depletion, and sPLA₂ activity at peak ALI. ALI was induced in BALB/c mice by intratracheal lipopolysaccharide (IT-LPS). Markers of ALI, surfactant (function, recovery, and composition), and sPLA₂ activity were assessed over a 240-h period encompassing peak ALI and resolution. During peak ALI, a separate cohort of IT-LPS mice received IT-varespladib, an sPLA₂ inhibitor, with surfactant outcomes analyzed 4 h later. IT-LPS induced features of ALI, including immune cell influx, protein leak, histological injury, and respiratory dysfunction, which peaked at 48-96 h and resolved by 240 h. Impaired surfactant function at peak ALI was associated with increased sPLA₂-mediated PG hydrolysis and reduced PG content. All changes were absent post-ALI resolution. Varespladib reduced alveolar sPLA₂ activity, increased surfactant PG, and improved surfactant function compared to untreated LPS controls. At peak ALI after IT-LPS, depletion of PG is synchronously related to surfactant dysfunction and increased sPLA₂ hydrolysis. Pharmacologic inhibition of sPLA₂ at peak ALI improves PG content and surfactant function. Additional substudies to fully examine their relationships and mechanisms are warranted.

News (Medical) associated with Varespladib

23 Oct 2024

·www.biospace.com

Ophirex Publishes Phase 2 Data in BMJ Global Health from the First Use of Varespladib to Treat Venomous Snakebite Victims

Efficacy signal observed in subgroup of victims treated within five hours of bite reinforces critical importance of timely treatment and need for a field therapy that could improve patient outcomes Globally, 75% of deaths from venomous snakebites occur before the victim can reach appropriately-equipped medical care CORTE MADERA, Calif.--(BUSINESS WIRE)--Ophirex, Inc., a Public Benefit Corporation developing an oral treatment to address the unmet medical needs of snakebite victims globally, today announced that BMJ Global Health has published data from the company’s BRAVO trial evaluating oral varespladib. Varespladib is a small synthetic molecule that directly inhibits secretory phospholipase A2 (sPLA2), an enzyme that is present in more than 95% of all snake venoms. The oral form is being developed as an early intervention treatment for patients and has potential to be the first-ever field therapy for snakebite envenoming, providing treatment at “time-of-bite.” The article in BMJ Global Health details results from BRAVO (Broad-spectrum Rapid Antidote: Varespladib Oral for snakebite), a multi-center, randomized, double-blind, placebo-controlled, Phase 2 study designed to evaluate the safety, tolerability and efficacy of oral varespladib. It enrolled 95 patients in the U.S. and India who were administered either varespladib or placebo in conjunction with the standard of care, which included antivenom in 93 of the 95 patients. “The BRAVO trial set out to do something no one has done before. In addition to being the first study to evaluate a direct toxin inhibitor for the treatment of snakebites, BRAVO was the first clinical trial to enroll patients bitten by any species of snake across two continents, including some of the world’s deadliest species,” said Timothy Platts-Mills, M.D., MSc, Chief Medical Officer of Ophirex. “While this Phase 2 study did not meet its primary endpoint, a promising signal of benefit was seen in the group of patients receiving treatment within five hours of a bite, reinforcing varespladib’s potential as an early treatment option and suggesting initial utility as a field treatment.” For the early treatment subgroup, clinically important differences were observed across important outcomes, such as lower illness severity over the first week, higher rates of complete recovery, and improved patient-reported function in patients receiving varespladib. Results from the BRAVO trial also suggest that varespladib is safe and well tolerated for the treatment of snakebite, adding to a robust body of safety data for this therapeutic candidate. “Antivenom, the current standard of care for snakebites, has several limitations, including the need to match antivenom to specific snake types, the risk of anaphylaxis, and the need to be administered intravenously in a medical setting. Yet we know that 75% of deaths due to venomous snakebites occur before the victim ever reaches the hospital. Even in those patients who survive, early treatment leads to better outcomes,” said Charles J. Gerardo, M.D., Professor and Chair for the Department of Emergency Medicine at Duke University and BRAVO trial investigator. “These data represent an encouraging advancement for patients bitten by snakes with the potential to fill a significant unmet need as a real world, early treatment before a patient reaches a healthcare facility.” “India has the greatest snakebite burden in the world, and 97% of snakebite deaths in the country occur in rural areas far from medical care and current treatments. A novel therapeutic molecule such as oral varespladib in addition to standard of care has the potential to enable treatment at the time of bite or en route to a more advanced facility and could be an important improvement in care for patients and medical systems alike,” said Dr. Suneetha D.K., Professor and Head of Internal Medicine, Mysore Medical College and Research Institute, Mysuru and a BRAVO trial investigator. “These findings support Ophirex’s vision to advance varespladib initially as an oral field treatment available at the time of the bite. We look forward to applying key learnings from this clinical trial to ongoing studies that address the long unmet need for a field treatment,” said Matthew R. Lewin, MD, PhD, Chief Scientific Officer and Founder of Ophirex, who first published the concept of this molecule as a field treatment in snakebite in 2016. The manuscript, titled “Oral Varespladib for the Treatment of Snakebite Envenoming in India and the United States (BRAVO): A Phase 2 Randomised Clinical Trial,” is available online here . About Ophirex Ophirex is a Delaware Public Benefit Corporation developing a first-of-its-kind oral treatment to address the global unmet need of venomous snakebites. Worldwide, there are approximately 500,000 cases of snakebite envenoming resulting in death or permanent disability each year. While antivenom has been the standard of care to treat these bites for more than 100 years, it can only be administered in a hospital setting. This poses a significant challenge as 75% of deaths from venomous snakebites occur before the victim can reach appropriately equipped medical care. Ophirex is advancing its investigational treatment, varespladib, as a broad-spectrum treatment for snakebite in both oral and intravenous formulations with human and veterinary applications. Ideally taken immediately following a bite, it is intended to provide a bridge to survival between bite and arrival to the hospital. If successful, this early intervention is anticipated to result in improved overall outcomes for patients at risk of death and long-term disability from snakebite. The company has presented some of the BRAVO data at scientific conferences. Ophirex is concluding a separate Phase 2 study to evaluate IV-to-oral dosing of varespladib for snakebite envenoming based on learnings from BRAVO. For more information, visit . Contacts Media Contact: Emma Yang Health+Commerce emma@healthandcommerce.com 908-391-7197

Phase 2Clinical Result

07 May 2024

·www.sciencedaily.com

First effective treatment found for spitting cobra snakebite

Scientists have discovered a new snakebite treatment to prevent the devastating tissue damage caused by African spitting cobra venom. Spitting cobra venom is incredibly potent and causes dermonecrosis, which presents as rapid destruction of skin, muscle and bone around the site of the snakebite, and can lead to permanent injuries and disfigurements, including limb loss and amputations in extreme cases. Using the repurposed small molecule drug varespladib to block one of the two major dermonecrosis-causing toxins in spitting cobra venom prevents skin and muscle damage. Each year, it is estimated that snakebite causes long term detrimental effects in around 400,000 people across the world, with a substantial proportion of those in Africa the result of spitting cobra bites. Scientists have discovered a groundbreaking new snakebite treatment to prevent the devastating tissue damage caused by African spitting cobra venom. Spitting cobra venom is incredibly potent and causes dermonecrosis, which presents as rapid destruction of skin, muscle and bone around the site of the snakebite, and can lead to permanent injuries and disfigurements, including limb loss and amputations in extreme cases. Professor Nicholas Casewell and Liverpool School of Tropical Medicine colleagues including Dr Steven Hall -- who is now at Lancaster University- discovered that using the repurposed small molecule drug varespladib to block one of the two major dermonecrosis-causing toxins in spitting cobra venom prevents skin and muscle damage. Each year, it is estimated that snakebite causes long term detrimental effects in around 400,000 people across the world, with a substantial proportion of those in Africa the result of spitting cobra bites. Currently, there is no effective treatment for tackling severe local envenoming caused by spitting cobra venom. Existing antivenoms only work on bites by other snake species and are often ineffective for treating local envenoming because antivenom antibodies are too large to effectively penetrate into the region around the bite site. Professor Nicholas Casewell of LSTM said: "Our findings hold much promise to improve the treatment of tropical snakebite. Current treatments for spitting cobra bites are widely regarded as being ineffective, meaning that rates of disability and amputation have remained high across much of Africa. Our data shows that blocking just one of the main toxin families in spitting cobra venom will likely prevent the debilitating tissue damage seen in thousands of snakebite patients each year." Professor Casewell's team, led by PhD student Keirah Bartlett and Dr Steven Hall, then of LSTM and now at Lancaster University, and also involving researchers from Canada, Denmark, Costa Rica and the USA, first analysed spitting cobra venom to identify the toxins responsible for causing venom-induced dermonecrosis. The results showed that cytotoxic three-finger toxins (CTx) are largely responsible but that phospholipases A2 (PLA2) toxins play a critical role in the process. Local injection of the PLA2-inhibiting drug varespladib reduced the extent of dermonecrosis, even when delivered up to an hour after the venom, and the protection conferred by the drug also extended to venom-induced muscle toxicity. According to the authors, the findings suggest that varespladib could become an invaluable treatment against the tissue-damaging effects of black-necked and red spitting cobra venoms, which cause extensive morbidity in snakebite victims across the African continent. Lead author Keirah Bartlett said: "These findings are extremely promising, not only does this offer up a new mode of treatment where previously nothing effective existed, but because varespladib has already gone through testing in human clinical trials, including for snakebite, it could be available for use in real world patients very soon." Dr Hall added: "Snakebite is a devastating neglected tropical disease, with tissue destruction caused by necrotic snake venoms permanently injuring hundreds of thousands of victims every year. Our work shows that the repurposed drug, Varespladib, is incredibly effective at inhibiting such necrosis caused by African spitting cobras; an exciting finding as their venoms are particularly fast-acting and destructive. We hope this work helps pave the way to future snakebite therapies that can save the lives and limbs of victims worldwide." Professor Casewell's team are already looking for viable treatments that effectively block the venom CTx. Having treatments available against both toxins has the potential to enhance the potency of varespladib, and could significantly reduce the long-term morbidity associated with spitting cobra bites in Africa and beyond.

Clinical Result

06 Dec 2011

·www.biospace.com

Anthera Pharmaceuticals, Inc. Promotes Dr. Debra Odink to Chief Technology Officer

HAYWARD, Calif., Dec. 5, 2011 /PRNewswire/ -- Anthera Pharmaceuticals, Inc. (Nasdaq: ANTH), a biopharmaceutical company developing therapeutics to treat serious diseases associated with inflammation and autoimmune disorders, today announced Dr. Debra Odink has been promoted to the role of Chief Technology Officer and Senior Vice President. "Over the past several years, Debra's increasing roles, responsibility and scientific leadership has been critical to the success of Anthera's development programs," said Paul F. Truex, President and Chief Executive Officer. "As Chief Technology Officer, Debra's strong oversight will continue to drive the advancement and execution of our corporate strategy." Dr. Odink joined Anthera in 2005 and has been serving as the Senior Vice President of Pharmaceutical Research and Development since that date. She has over eighteen years of global pharmaceutical chemistry and product development experience. Prior to joining Anthera, she served as the Vice President of Product and Process Development at Peninsula Pharmaceuticals where she was responsible for the company's manufacturing and product development strategies for assets licensed to the company. Additionally, she has held various positions at Elan Pharmaceuticals and Roche where she contributed to development efforts for multiple new drug candidates. Dr. Odink holds various patents for novel drug formulations and is author of multiple publications. She obtained her Bachelor of Science in Chemistry at California State University Stanislaus and her Ph.D. in Inorganic Chemistry at the University of California Davis. About Anthera Pharmaceuticals Anthera Pharmaceuticals is a biopharmaceutical company focused on developing and commercializing products to treat serious diseases associated with inflammation, including cardiovascular and autoimmune diseases. Anthera has one Phase 3 clinical program, A-002, and two Phase 2 clinical programs, A-623 and A-001. A-002 and A-001 inhibit a novel enzyme target known as secretory phospholipase A2, or sPLA2. Elevated levels of sPLA2 have been implicated in a variety of acute inflammatory conditions, including acute coronary syndrome and acute chest syndrome, as well as chronic diseases such as stable coronary artery disease, or CAD. Anthera's Phase 2 product candidate, A-623, targets elevated levels of B-lymphocyte stimulator, or BLyS, which has been associated with a variety of B-cell mediated autoimmune diseases, including systemic lupus erythematosus, or lupus. For more information, please visit . Safe Harbor Statement Any statements contained in this press release that refer to future events or other non-historical matters, including statements that are preceded by, followed by, or that include such words as "estimate," "intend," "anticipate," "believe," "plan," "goal," "expect," "project," or similar statements, are forward-looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are based on Anthera's expectations as of the date of this press release and are subject to certain risks and uncertainties that could cause actual results to differ materially as set forth in Anthera's public filings with the SEC, including Anthera's Annual Report on Form 10-K for the year ended December 31, 2010 and Quarterly Report on Form 10-Q for the quarter ended September 30, 2011. Anthera disclaims any intent or obligation to update any forward-looking statements, whether because of new information, future events or otherwise, except as required by applicable law. CONTACT: Bianca Nery of Anthera Pharmaceuticals, Inc., bnery@anthera.com or 510.856.5586. SOURCE Anthera Pharmaceuticals, Inc.

100 Deals associated with Varespladib

External Link

KEGG	Wiki	ATC	Drug Bank
D08221	Varespladib	-	DB05737

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Acute Coronary Syndrome	Phase 3	United States	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Australia	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Canada	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Czechia	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Georgia	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Germany	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Hungary	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	India	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Italy	Anthera Pharmaceuticals, Inc.	01 May 2010
Acute Coronary Syndrome	Phase 3	Lebanon	Anthera Pharmaceuticals, Inc.	01 May 2010

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05717062 (Pubmed \| J Am Vet Med Assoc)	Phase 2	Snake Bites	3	Varespladib + Varespladib antivenom (Eastern coral snake envenomation)	thqotrnknz(mitsdvzefj) = No adverse effects were attributed to varespladib or antivenom administration. cpoumzhenh (slssdeaqjn )	Positive	01 Dec 2025
NCT04996264 (BRAVO, CTgov)	Phase 2	Snake Bites	95	Standard of care (SOC)+Varespladib Methyl (Varespladib-methyl)	mlybjqxcrj(stmrtuqdpw) = ycmamruscy kuyjcwxfcy (kvvebbxtes, 0.3) View more	-	01 Jul 2025
				Placebo (Placebo)	mlybjqxcrj(stmrtuqdpw) = wjdnpqripc kuyjcwxfcy (kvvebbxtes, 0.2) View more
NCT04969991 (STAIRS, CTgov)	Phase 2	COVID-19	18	Placebo+Varespladib (Varespladib: 250 mg QD + Placebo + Placebo)	glrrhslnbd = llmvemocof agqwoupdlc (glgxilwvmi, xotmlsiokr - waloqfqhwm) View more	-	15 May 2025
				Placebo+Varespladib (Varespladib: 250 mg BID + Placebo)	glrrhslnbd = rliaodgfiq agqwoupdlc (glgxilwvmi, ijvlwdkmeb - mleaflmewb) View more
NCT01130246 (VISTA-16, Pubmed \| JAMA)	Phase 3	Acute Coronary Syndrome	5,145	Varespladib	mpgcbquxih(mxwrnsmubw) = lvedzxmpkd krvxiodyfn (ukjjqznnuw ) View more	Negative	15 Jan 2014
				Placebo	mpgcbquxih(mxwrnsmubw) = mtxzrlwtpf krvxiodyfn (ukjjqznnuw ) View more
NCT00533039 (SPIDER-PCI, Pubmed \| Circulation)	Phase 2	troponin I \| creatine kinase-MB \| high-sensitivity C-reactive protein ... View more	144	Varespladib 500 mg	kphxavsjpt(uzkvzfwsow) = ncnuwmmexk heymmkkaus (ztdygmelcf )	Negative	07 Dec 2010
				Placebo	kphxavsjpt(uzkvzfwsow) = dxirmsrvcz heymmkkaus (ztdygmelcf )
NCT00743925 (FRANCIS-ACS, Pubmed \| J Am Coll Cardiol)	Phase 2	Acute Coronary Syndrome	625	Varespladib 500 mg	cqvyitetyl(pwvhppirqc) = lcnjfsrtrw gdqdyoklkk (qqaymnaxgt ) View more	Positive	28 Sep 2010
				Placebo	cqvyitetyl(pwvhppirqc) = wkmqhgvqcd gdqdyoklkk (qqaymnaxgt ) View more
NCT00455546 (Pubmed \| Lancet)	Phase 2	Coronary Artery Disease \| Atherosclerosis	393	Placebo	rdvrpnoobu(chspymzmyb) = fysifemrow zofwhyvlae (cquwynnuqm )	Positive	21 Feb 2009
				A-002 50 mg	rdvrpnoobu(chspymzmyb) = ksnuiqqgkx zofwhyvlae (cquwynnuqm )

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Hiro LS Researcher

The AI Search Engine Built to Accelerate Biopharma Decisions

Search across billion-scale life sciences data to uncover signals, validate evidence, and act with confidence.

Ask any biopharma research question→

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, Patsnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Discover Synapse Data Servers

Synapse data is now integrated into the PatSnap LS Model Context Protocol (MCP) service. Customize your LLM agent now using our MCP server!

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis