Tinnitus represents one of the most common and distressing otologic problems, and it causes various somatic and psychological disorders that interfere with the quality of life. Despite too many research projects on finding the mechanism of tinnitus, its pathophysiology remains poorly understood. It is well understood that many factors, such as poor education, lower income, or occupational, and recreational activity associated with high noise exposure, influence the prevalence and risk of tinnitus. Although the economic and emotional impact of tinnitus is large, there is currently no FDA-approved medication to treat this condition. However, there are pharmacological options to address the stress, anxiety, and depression that are caused by tinnitus. In this project, the investigators intend to use medications for patients with acute tinnitus to decrease the impact of tinnitus in their daily lives and activities. There are some studies on medications treating tinnitus; however, there are few randomized clinical trials to prove the efficacy of the treatment. The frequency and loudness of tinnitus will be measured before and after the course. Functional MRI of the brain will be obtained to view any changes that may occur before and after the treatment.

Start Date01 Jun 2025

Sponsor / Collaborator

University of California, Irvine

NCT06763484

/ RecruitingPhase 2IIT

Paroxetine Versus Placebo for Vasomotor Symptom Management in Surgical Menopause. Randomized Double-blind Clinical Trial

evaluate the efficacy of paroxetine in the management of vasomotor symptoms in patients with surgical menopause, in order to seek an alternative therapy to hormone therapy, which is associated with proinflammatory and procoagulant effects that increase the risk of thrombosis and is therefore contraindicated in people with diabetes mellitus, chronic arterial hypertension and patients with a history of thromboembolism

Start Date01 Jan 2025

Sponsor / Collaborator

National Autonomous University of Honduras

CTR20244270

/ CompletedNot Applicable

一项随机、开放、单剂量、两周期、双交叉、空腹和餐后给药临床研究，评价盐酸帕罗西汀片与赛乐特在中国健康成年参与者中的生物等效性

[Translation] A randomized, open-label, single-dose, two-period, double-crossover, fasting and fed administration clinical study to evaluate the bioequivalence of paroxetine hydrochloride tablets and Seroxat in healthy Chinese adult participants

主要目的：以深圳市新阳唯康科技有限公司持有的盐酸帕罗西汀片（20mg）为受试制剂，按生物等效性试验的有关规定，与葛兰素史克（天津）有限公司持有的盐酸帕罗西汀片（商品名：赛乐特，规格：20mg）为参比制剂，进行生物等效性试验，比较两种制剂在空腹和餐后条件下单次给药的生物等效性。次要目的：评估单剂量口服受试制剂（盐酸帕罗西汀片，T）和参比制剂（赛乐特，R）在中国健康成年参与者中的安全性。

[Translation]

Main purpose: Paroxetine hydrochloride tablets (20 mg) held by Shenzhen Xinyang Weikang Technology Co., Ltd. were used as the test preparation. According to the relevant provisions of bioequivalence tests, paroxetine hydrochloride tablets (trade name: Seroxetine, specification: 20 mg) held by GlaxoSmithKline (Tianjin) Co., Ltd. were used as the reference preparation for bioequivalence tests to compare the bioequivalence of the two preparations under fasting and postprandial conditions. Secondary purpose: Evaluate the safety of single-dose oral test preparations (paroxetine hydrochloride tablets, T) and reference preparations (Seroxetine, R) in healthy adult participants in China.

Start Date12 Dec 2024

Sponsor / Collaborator

Nycrist Pharmatech Ltd.

100 Clinical Results associated with Paroxetine Hydrochloride

100 Translational Medicine associated with Paroxetine Hydrochloride

100 Patents (Medical) associated with Paroxetine Hydrochloride

8,776

Literatures (Medical) associated with Paroxetine Hydrochloride

01 Aug 2025·NEUROPHARMACOLOGY

Chronopharmacokinetics of the antidepressant paroxetine: An in vitro and in vivo approach

Article

Author: Falcão, Amílcar ; Dallmann, Robert ; Bicker, Joana ; Fortuna, Ana ; Silva, Soraia

The circadian rhythm influences homeostatic functions such as sleep, physical activity and food intake as well as pharmacotherapy, namely pharmacokinetics. To investigate the impact of the circadian rhythm on the pharmacokinetics of paroxetine, in vitro synchronized permeability studies were carried out in a tri-culture blood-brain barrier model. Paroxetine demonstrated lower apparent permeability when the cells were incubated at 24 h post-synchronization than at 36 h. Additionally, in vivo chronopharmacokinetic studies were performed in CD-1 female mice administered with paroxetine (5 mg/kg) by intranasal route in the early morning or evening. Paroxetine exposure in the brain was higher when it was administered at the beginning of the active phase (ZT13) compared with the rest phase (ZT1) (p < 0.001), probably owing to the lower levels of P-glycoprotein expressed in the brain at the active phase (p < 0.05). Since melatonin production depends on serotonin, its plasma concentrations were also assessed in vivo. The results demonstrated that melatonin concentrations increased 12 h after paroxetine nasal instillation at ZT13 (p < 0.05), but remained unchanged at ZT1, suggesting that the drug effect is influenced by administration time. In conclusion, the circadian rhythm impacted the pharmacokinetics of paroxetine, especially its distribution into the brain, the target organ. This emphasizes the importance of the time of administration in antidepressant dosing, highlighting its relevance for future studies.

01 Aug 2025·PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR

Administration of paroxetine during pregnancy affects behavioral changes and hippocampal cell proliferation in male offspring in rats

Article

Author: Horie, Junko ; Suzuki, Toshihito ; Ito, Masanobu ; Kinjo, Tomoya

BACKGROUND:

Although the use of antidepressants during pregnancy has increased over the last several decades, their safety has remained a topic of debate. Selective serotonin reuptake inhibitors (SSRIs) can cross the placenta and affect perinatal outcomes in infants exposed during pregnancy. Recent studies suggest new risks for not only for structural malformations, but also long-term behavioral, developmental, and emotional disorders in offspring.

AIM:

We aimed to elucidate the effects by which in utero paroxetine exposure may affect the behavior and hippocampus of the offspring of paroxetine-treated rodent mothers.

METHODS:

Paroxetine was administered daily to pregnant female Wistar rats from embryonic day (ED) 12.5 to ED 21 with oral sondes. Paroxetine 1 mg/kg/day or paroxetine 2.5 mg/kg/day or saline was given to the control group. We evaluated spontaneous locomotor activity, spontaneous alternation behavior using the Y-maze test, and anxiety behavior using the elevated plus maze (EPM) in male offspring at postnatal day 30. Bromodeoxyuridine (BrdU)-positive cells in the hippocampus were counted using a fluorescence microscope.

RESULTS:

Locomotor activities significantly increased in the paroxetine 2.5 mg compared with the control group. The paroxetine 2.5 mg group spent less time in the closed arm than did the control and paroxetine 1 mg groups in the EPM. The number of BrdU-positive cells in the dentate gyrus was significantly increased in the paroxetine 2.5 mg compared with the control group.

CONCLUSIONS:

These findings suggest that oral administration of paroxetine during pregnancy induces hyperactivity, decreases anxiety, and increases cell proliferation in the hippocampus of male offspring.

01 Jun 2025·MARINE POLLUTION BULLETIN

Assessment of the effects of paroxetine and zinc on crustaceans through integrated quantitative and taxon/functional tools with a focus on free-living marine copepods and amphipods

Article

Author: Elfalleh, Walid ; Allouche, Mohamed ; Ishak, Sahar ; Boufahja, Fehmi ; Lassoued, Amal ; Hamadi, Naoufel Ben ; Hedfi, Amor ; Ali, Mohamed A M ; Bendif, Hamdi ; Badraoui, Riadh

This experiment examined the individual and combined effects of the antidepressant paroxetine and zinc on copepods and amphipods collected from Jeddah coast in Saudi Arabia. Various treatments were tested, revealing a decline in the abundance and diversity of both groups. Specific sensitivities were noted for copepods: Amphiascus parvulus was particularly affected by paroxetine, while Harpacticus littoralis, Harpacticus gracilis, and Heterolaophonte stroemii stroemii showed increased sensitivity to zinc. In amphipods, Microdeutopus algicola was most impacted across treatments, and Ampithoe ramondi and Nototropis massiliensis were more sensitive in mixed conditions. The study found significant synergistic effects when both pollutants were present, leading to greater reductions in meiofaunal abundance and diversity. The impacts noticed were further supported by in silico modeling focusing on both GH7 Family Cellobiohydrolase (4XNN) and Arginine Kinase wild type (6KY2) derived from Daphnia as a crustacean model.

News (Medical) associated with Paroxetine Hydrochloride

07 Apr 2025

·www.biospace.com

Opinion: AI Enables Companies to Break From the Herd in Drug Development

shiota/ iStock Researchers in pharma and beyond have historically glommed onto a limited number of disease targets, limiting innovation. AI could change that. Proteins that fight tumor growth, gene exons that can be modified, and receptors on immune cells that control their cancer-killing powers. These are the types of mechanisms and bodily processes that could be key to curing or treating disease, and which form the targets of modern drug development. While the number of such targets is nearly infinite, a relatively small number have emerged as the most popular among pharmaceutical companies. In a phenomenon termed “herding,” numerous pharmaceutical firms, research organizations and even academic scientists are targeting not just the same narrow band of conditions, but the same limited set of drug targets. In 2020, 68% of targets pursued by the top 10 pharmaceutical firms were the basis of five or more R&D programs. Some firms were dedicating 80% or more of their research time and dollars to those popular targets. Chief among these targets are those associated with cancer; in 2022, there were nine assets per actively investigated oncology target among the top pharma firms, up from 1.8 in 2000, with most of the research dedicated to breast, hematological and brain cancer. While there are understandable reasons for herding and even advantages in certain situations, the overall effect of this “me-too” style of innovation is to set limits in drug development. But how can we break away from the crowd and forge our own path? As vice president of business development at Evogene, which offers an AI-driven computational chemistry platform, I believe artificial intelligence is the answer. AI has the power to transform drug development by identifying novel targets and compounds that can interact with them. The Drawbacks of Herding Well-known examples of “me-too” drugs include many of the selective serotonin reuptake inhibitors (SSRIs) used in treating depression—such as Prozac, Zoloft and Paxil—and various statins—think Lipitor and Crestor. One of the most comprehensive studies of drug targets curated 1,578 FDA-approved drugs acting on 893 unique molecular targets, meaning nearly 50% of FDA-approved drugs share common targets. Similarly, about 60% of drugs on the World Health Organization’s list of essential treatments fit into this “me-too” category, and more than 50% of the 50 novel drugs approved by the FDA in 2024 relied on pre-existing targets. In many ways, herding makes sense, and it has benefitted some patients and pharma companies. Many of the targets that experience herding, especially in the oncology space, are highly efficacious, and pharma firms want to follow what works and, ideally, create best-in-class treatments in these drug classes. Of course, there is a great demand—and a large need—for these improvements. In addition, when it comes to single-gene diseases such as thalassemia, Duchenne muscular dystrophy and Huntington’s, herding has emerged alongside progress in developing gene therapies. For example, instead of focusing solely on the mutant gene, companies might look at targeting cellular pathways disrupted by the mutant protein. Such approaches make up only 10%–30% of attempts to develop new therapies, while the majority still focus on the mutant gene itself. Such concentrated research efforts, exemplified by the focus on the CFTR gene in cystic fibrosis leading to therapies like Ivacaftor, can indeed accelerate progress in understanding and treating rare genetic diseases. But the focus on the gene itself and a small set of cellular pathways leaves other pathways under explored. This over-concentration diverts critical resources, exacerbating challenges in resource allocation and clinical trial design and ultimately hindering efforts to pursue novel targets and more innovative therapies. This is especially problematic for rare diseases, where the pool of trial participants is naturally low and standards limit patients to one trial at a time. If all or most of the patients are enrolled in trials testing drugs with the same target or few targets, there is little room to open a trial with a new target, further discouraging innovation. Innovation Through AI Pursuing new targets and therapies is essential to reversing the herding trend, and one of the tools for doing this is AI. AI offers the ability to navigate the vast chemical and biological landscape, uncovering hidden patterns and relationships that traditional methods overlook. By integrating data from genomics, proteomics and cheminformatics, AI can identify novel targets that have been underexplored, evaluating their potential with remarkable speed and accuracy. Over the past three years the market for AI platforms for the entire healthcare industry has tripled . As more companies— and regulators —embrace AI-based research, companies will be better equipped to break free from the constraints of herding and the redundancy of structurally similar drugs, shifting toward more innovative and diverse therapeutic strategies. McKinsey predicts that AI could increase the number of actionable drug targets by at least 30% . There are already signs of progress in de-herding as novel biological targets and molecules for drug development emerge. For example, AstraZeneca, in collaboration with BenevolentAI, has identified novel targets in chronic kidney disease (CKD) beyond the well-known renin-angiotensin system, opening pathways to treatments focused on kidney fibrosis and inflammation. AI-based research by Verve Therapeutics, meanwhile, has shifted from traditional statin targets to gene editing therapies for inherited cardiovascular conditions. And for rare diseases, including amyotrophic lateral sclerosis (ALS) and Duchenne muscular dystrophy, companies like Insilico have utilized AI-driven systems to identify specific genetic targets. In addition to finding new targets, deep learning enables the de novo design of novel ligands, the active molecules that are the basis of many potential new drugs. Generative architectures such as GANs (generative adversarial networks), VAEs (variational autoencoders) and GPTs (generative pre-trained models) allow researchers to create unique molecular structures that are specifically tailored to their targets. This capability is transformative because it avoids the redundancy of relying on existing compound libraries, which are often biased toward known targets. AI-driven de novo ligand generation explores new chemical spaces, ensuring structural diversity and reducing the risk of producing yet another version of an existing drug. Companies like Atomwise , Insilico and Recursion are using AI for structure-based drug design, and have discovered unique ligands for various indications. Evogene recently began to leverage its AI-driven computational chemistry platform, first developed for agricultural applications, to break into the world of novel ligand discovery and drug development. Despite its promise, AI-driven drug discovery faces challenges such as variable data quality and the “black box” nature of some models, which can complicate validation and regulatory approval. While the promise of AI-first drugs is yet to be fully realized—none have progressed beyond Phase II clinical trials due to long development timelines—it’s important to note that the most advanced drugs in the pipeline were created using technology that has since matured rapidly. These issues are recognized as part of an evolving field, with ongoing innovation addressing concerns like data standardization and model transparency. I have strong confidence that these hurdles will be overcome in time, ultimately enabling AI to revolutionize drug development and improve patient outcomes. AI use in the pharmaceutical industry is far from universal, but by collaborating with AI-first companies, pharmas can remain at the forefront of technological advancements, ensuring their pipelines are fueled by cutting-edge breakthroughs rather than incremental advances. As AI-driven research becomes the norm, fuelled by these strategic collaborations, we can anticipate transformative progress that will benefit pharmaceutical companies and patients alike.

Gene TherapyPhase 2

31 Mar 2025

·www.prnewswire.com

Transcend Therapeutics Announces Primary Endpoint Met in IMPACT-1 Phase 2 Study of TSND-201 in PTSD

Primary endpoint met, with TSND-201 demonstrating statistically significant placebo-adjusted CAPS-5 improvement of -9.64 points on Day 64 (p = 0.011) TSND-201 demonstrated rapid improvements, with a statistically significant placebo-adjusted CAPS-5 improvement of -8.00 points on Day 10 (p = 0.012), with placebo-adjusted improvements remaining statistically significantly for the duration of the trial Robust and statistically significant improvements were noted across multiple secondary endpoints on Day 64 TSND-201 was generally safe and well tolerated, with a safety profile consistent with its non-hallucinogenic pharmacology Company plans to align with FDA on Phase 3 program for PTSD NEW YORK, March 31, 2025 /PRNewswire/ -- Transcend Therapeutics, a clinical-stage biotechnology company that develops medicines to treat neuropsychiatric diseases, today announced positive results from the IMPACT-1 study (Investigation of Methylone for Post-Traumatic Stress Disorder [PTSD]). IMPACT-1 was a randomized, double-blind, placebo-controlled, Phase 2 clinical trial evaluating TSND-201 (methylone), a rapid-acting neuroplastogen, for the treatment of PTSD. This study enrolled 65 patients with severe PTSD (Clinician-Administered PTSD Scale for DSM-5 [CAPS-5] ≥ 35), all of whom had previously tried a PTSD treatment, to receive 4 oral doses of TSND-201 or placebo, with each dose separated by one week. Patients were followed for a total of 64 days after the first dose. Continue Reading CAPS-5 Scores Over Time; * p <0.05 On the primary endpoint, change from baseline to Day 64, TSND-201 demonstrated a statistically significant placebo-adjusted CAPS-5 improvement of -9.64 points on Day 64 (-23.28 points vs. -13.64 points; p = 0.011). TSND-201 also demonstrated rapid and statistically significant improvements from baseline compared to placebo on the CAPS-5 total severity score. Starting on Day 10, TSND-201 demonstrated a statistically significant placebo-adjusted CAPS-5 improvement of -8.00 points (-17.83 points vs. -9.83 points; p = 0.012), which was durable throughout the study until Day 64. "We are encouraged by the positive Phase 2 results demonstrating TSND-201's potential as a rapid-acting and durable treatment for patients with PTSD," said Transcend Therapeutics Co-Founder and CEO Blake Mandell. "We look forward to working with the FDA to align on a Phase 3 program in PTSD." TSND-201 demonstrated statistically significant improvements on multiple secondary endpoints, including response (≥ 50% improvement from baseline on CAPS-5; 57.1% vs. 19.2%; p = 0.002), remission (≤ 11 points on the CAPS-5; 32.1% vs. 11.5%; p = 0.036), and loss of PTSD diagnosis (60.7% vs. 30.8%; p = 0.014). Treatment with TSND-201 was generally safe and well tolerated. The majority of adverse events were transient, occurring on the day of dosing and resolving the same day. The most commonly occurring adverse events in the TSND-201 group were headache, decreased appetite, nausea, dizziness, blood pressure increase, dry mouth, insomnia, muscle tightness, and feeling abnormal. One serious adverse event of seizure occurred in the TSND-201 group; the event occurred 7 days after the last dose in a patient with a history of seizure and was considered unrelated to study drug. "It has been over two decades without a new treatment for PTSD. The results of this study suggest that TSND-201 may represent a significant clinical breakthrough — demonstrating clinically meaningful efficacy with a rapid onset," commented Murray B. Stein, M.D., M.P.H., Distinguished Professor of Psychiatry and Public Health at the University of California San Diego and Staff Psychiatrist at the Veteran Affairs San Diego Healthcare System. "Rapid-acting, episodic treatments could be a paradigm shift in the treatment of PTSD, providing hope for the many patients who have struggled to find effective relief." About Transcend Therapeutics Transcend Therapeutics, founded in 2021, is a clinical-stage, neuroscience-focused company developing rapid-acting treatments for neuropsychiatric diseases. The company's mission is to develop new drugs for the millions of people for whom current psychiatric medicines have not worked. Transcend's leadership team has made pivotal contributions to 14 FDA approvals and $7B in M&A and public company value. Transcend has raised approximately $50M to date. About TSND-201 TSND-201, a rapid-acting neuroplastogen, is a proprietary formulation of methylone developed by Transcend Therapeutics. TSND-201 has well-characterized primary pharmacology, with its primary site of action at the monoamine transporters, and no activity at 5HT-2a (i.e., not hallucinogenic). Transcend is developing TSND-201 as a rapid-acting and durable treatment for PTSD and other central nervous system (CNS) indications. TSND-201 is an investigational medication. About PTSD PTSD is a mental health condition that can occur after experiencing or witnessing a life-threatening or traumatic event. Symptoms may include flashbacks, nightmares, severe anxiety, and uncontrollable thoughts about the event. PTSD impacts approximately 13 million Americans each year and it is estimated that nearly 7% of U.S. adults will be diagnosed with PTSD during their lifetime. Only two medications are FDA-approved for the treatment of PTSD (sertraline and paroxetine), yet their efficacy is modest at best. New treatments for PTSD are urgently needed. Contact: [email protected] SOURCE Transcend Therapeutics WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Clinical ResultPhase 2Drug ApprovalPhase 3

17 Mar 2025

·ir.cytokinetics.com

Cytokinetics Announces Five Presentations at the American College of Cardiology Annual Scientific Session & Expo

New Analyses Related to Aficamten Expand on its Metabolism Pathways, Treatment Effect Associated with Combination Therapy with Disopyramide and Longer-Term Effect on Cardiac Structure and Function SOUTH SAN FRANCISCO, Calif., March 17, 2025 (GLOBE NEWSWIRE) -- Cytokinetics, Incorporated (Nasdaq: CYTK) today announced five presentations related to aficamten, an investigational cardiac myosin inhibitor, and hypertrophic cardiomyopathy (HCM), at the American College of Cardiology (ACC) Annual Scientific Session & Expo taking place from March 29, 2025–March 31, 2025 in Chicago, IL. “We are pleased to be sharing several new analyses relating to aficamten at the upcoming ACC Scientific Session & Expo,” said Stephen Heitner, M.D., Vice President, Head of Clinical Research. “The presentations describe the drug metabolism of aficamten, the safety of combination therapy with the standard of care medication disopyramide, and the effect of longer-term use of aficamten. Together these analyses add to the strong and growing evidence base supporting the potential for aficamten in patients with obstructive HCM and inform how it may be used in clinical practice.” Evaluation of Cytochrome P450 2C9, 2C19, and 2D6 Inhibition on the Pharmacokinetics of Aficamten in Healthy Participants (1091-139) Poster Presentation, March 29, 2025, 2:00-3:00 PM CT, South Hall. Neha Maharao, Ph.D., Senior Clinical Pharmacologist, Cytokinetics. Data from an open-label, fixed-sequence drug-drug interaction (DDI) study of aficamten in healthy participants will be presented in a poster presentation. A previous study showed that aficamten is metabolized, in part, by the cytochrome P450 (CYP) enzyme 3A41. To further characterize its metabolic pathways, aficamten was evaluated with concomitant administration of three strong inhibitors of one or more of the CYP pathways: fluconazole (inhibitor of 2C9, 2C19, and 3A4), paroxetine (inhibitor of 2D6) and fluoxetine (inhibitor of 2C19 and 2D6). The data show that aficamten was eliminated by multiple CYP pathways, primarily by CYP2C9 (fraction metabolized [fm]=50%), with contributions from CYP3A (fm=26%), CYP2D6 (fm=21%) and CYP2C19 (fm=3%). Safety and Outcomes of Concomitant Aficamten and Disopyramide Use and Withdrawal in Patients with Obstructive Hypertrophic Cardiomyopathy: An Analysis of REDWOOD-HCM Cohort 3, SEQUOIA-HCM, and FOREST-HCM Trials (411-06) Oral Presentation, March 31, 2025, 9:11-9:18 AM CT, S406b. Ahmad Masri, M.D., MS, Director of the Hypertrophic Cardiomyopathy Center at Oregon Health & Science University. Data from an analysis of concomitant treatment with aficamten and disopyramide from completed and ongoing clinical trials of aficamten in patients with obstructive HCM will be presented in an oral presentation. The analysis included 50 participants from Cohort 3 of REDWOOD-HCM (Randomized Evaluation of Dosing With CK-274 in Obstructive Outflow Disease in HCM), SEQUOIA-HCM (Safety, Efficacy, and Quantitative Understanding of Obstruction Impact of Aficamten in HCM) and FOREST-HCM (Follow-up, Open-Label, Research Evaluation of Sustained Treatment with Aficamten in HCM) who were receiving disopyramide at baseline. Participants were separated into four groups: those on disopyramide who underwent withdrawal of aficamten due to end of treatment in Cohort 3 of REDWOOD-HCM or SEQUOIA-HCM (n=29), patients on disopyramide receiving placebo in SEQUOIA-HCM (n=20), patients on aficamten who underwent disopyramide withdrawal in FOREST-HCM (n=17) and patients on aficamten who maintained treatment with disopyramide in FOREST-HCM (n=27). Combination therapy with aficamten and disopyramide was well-tolerated; the analysis suggests that combination of disopyramide with aficamten did not result in lower left ventricular outflow tract (LVOT) gradients compared to treatment with aficamten alone. The analysis suggests that withdrawal of disopyramide while receiving aficamten did not reduce the efficacy of aficamten and further that withdrawal of aficamten while on disopyramide resulted in the return of LVOT obstruction and symptoms, with an increase in NT-proBNP. There were no safety events reported with either aficamten or disopyramide withdrawal, and no episodes of atrial fibrillation after disopyramide withdrawal were reported. Effect of Aficamten Treatment for Up to 72 Weeks on Cardiac Structure and Function in Patients with Obstructive Hypertrophic Cardiomyopathy: The SEQUOIA-HCM and FOREST-HCM CMR Sub-studies (964-09) Moderated Poster Presentation, March 30, 2025, 12:06-12:13 PM CT, Theater 5. Ahmad Masri, M.D., MS, Director of the Hypertrophic Cardiomyopathy Center at Oregon Health & Science University. New data from the cardiac magnetic resonance (CMR) imaging sub-studies of FOREST-HCM and SEQUOIA-HCM will be presented in a moderated poster presentation. At the time of the current analysis, 64 patients had completed a baseline CMR, including 36 patients who had completed a follow-up CMR at 72 weeks, and 28 patients who had completed a follow-up CMR at 48 weeks. Longer-term treatment with aficamten resulted in statistically significant improvements (mean ±SD) in measures of cardiac structure and function including left ventricular mass index (-9.8 g/m2 ±18.1, p<0.0001), maximum left ventricular septal wall thickness (-2.4 mm ±2.3, p<0.0001), left atrial volume (-17.9 ml ±28.3, p<0.0001) and mitral regurgitant volume (-18.1 ml ±19.2, p<0.0001) and fraction (-14.2% ±15.6, p<0.0001). These changes were accompanied by stable replacement fibrosis (late gadolinium enhancement mass = -0.3 g ±5.0, p=0.51) and reduced interstitial fibrosis (global extracellular volume (ECV) = -1.2 % ±2.8, p = 0.002; Native T1 = -36.6 ms ±55.7, p<0.0001). Understanding the Impact of Placebo on Patient-Reported Health Status: An Analysis from SEQUOIA-HCM (1029-176) Poster Presentation, March 29, 2025, 9:30-10:30 AM CT, South Hall. Charles F. Sherrod, M.D., M.Sc., Cardiology Fellow, UMKC Healthcare Institute for Innovations in Quality, Saint Luke’s Mid America Heart Institute. A new analysis from SEQUOIA-HCM of the placebo effect on Kansas City Cardiomyopathy Questionnaire Overall Summary Scores (KCCQ-OSS) will be presented in a poster presentation. In patients randomized to placebo in SEQUOIA-HCM, the change in KCCQ-OSS was evaluated from baseline to Week 24 and following blinded treatment withdrawal from Week 24 to Week 28. Among the 140 (47%) patients on placebo, the median KCCQ-OSS at baseline was 67.2 (95% CI: 62.9, 71.5) and the median improvement at Week 24 was 5.7 points (95% CI: 3.2, 8.3; p<0.01). After withdrawal from Week 24 to Week 28, the median score decreased by only 2.1 points (95% CI: -3.5, -0.7; p<0.01). These results suggest that about one-third of the improvement observed in KCCQ-OSS in patients receiving placebo was due to a placebo effect, further suggesting that other changes in health status following treatment with placebo may be due to other factors involved in clinical trial participation, such as receiving treatment at expert centers and changes in patient behavior. Association Between Race/Ethnicity and Outcomes in Patients with Non-Obstructive Hypertrophic Cardiomyopathy (1251-173) Poster Presentation, March 31, 2025, 10:30-11:30 AM CT, South Hall. Nosheen Reza, M.D., Assistant Professor of Medicine, Division of Cardiovascular Medicine, the Hospital of the University of Pennsylvania. Data from a new health economics and outcomes research (HEOR) analysis of the association between race/ethnicity and outcomes in non-obstructive HCM patients will be presented in a poster presentation. This retrospective cohort study included adult patients diagnosed with non-obstructive HCM from January 1, 2013 to December 31, 2021. Of the 9,842 patients included, 74.2% were non-Hispanic white, 19.5% were non-Hispanic Black/African American, 4.2% were Hispanic and 2.1% were non-Hispanic Asian. White patients had greater rates of atrial fibrillation and cardiovascular hospitalization compared to Asian and Hispanic patients. Compared to white patients, Black patients had increased rates of stroke (risk ratio [RR] 1.76), heart failure (RR 1.73), ventricular tachycardia (RR 1.24), sudden cardiac arrest (RR 1.90), cardiovascular hospitalization (RR 1.42) and cardiovascular rehospitalization (RR 1.31) and a lower rate of atrial fibrillation (RR 0.74; all p<0.001). All-cause mortality was highest among Black patients (p<0.001). Compared to white patients, non-Hispanic Black patients had the highest rate of adverse cardiovascular outcomes and all-cause mortality, while Asian and Hispanic patients experienced lower rates. These results highlight an urgent need to address drivers of race/ethnicity-based disparities in patients with nHCM. About Aficamten Aficamten is an investigational selective, small molecule cardiac myosin inhibitor discovered following an extensive chemical optimization program that was conducted with careful attention to therapeutic index and pharmacokinetic properties and as may translate into next-in-class potential in clinical development. Aficamten was designed to reduce the number of active actin-myosin cross bridges during each cardiac cycle and consequently suppress the myocardial hypercontractility that is associated with HCM. In preclinical models, aficamten reduced myocardial contractility by binding directly to cardiac myosin at a distinct and selective allosteric binding site, thereby preventing myosin from entering a force producing state. The development program for aficamten is assessing its potential as a treatment that improves exercise capacity as measured by peak oxygen uptake (pVO2) and relieves symptoms in patients with HCM. Aficamten was evaluated in SEQUOIA-HCM, a positive pivotal Phase 3 clinical trial in patients with symptomatic obstructive hypertrophic cardiomyopathy (HCM). Aficamten received Breakthrough Therapy Designation for the treatment of symptomatic obstructive HCM from the U.S. Food & Drug Administration (FDA) and from the National Medical Products Administration (NMPA) in China. Aficamten is currently under regulatory review in the U.S, where the FDA is reviewing a New Drug Application (NDA) for aficamten, which was assigned standard review and a Prescription Drug User Fee Act (PDUFA) target action date of September 26, 2025. Additionally, the European Medicines Agency (EMA) is reviewing a Marketing Authorization Application (MAA) for aficamten, and The Center for Drug Evaluation (CDE) of the China National Medical Products Administration (NMPA) is reviewing an NDA for aficamten with Priority Review. Aficamten is also currently being evaluated in MAPLE-HCM, a Phase 3 clinical trial of aficamten as monotherapy compared to metoprolol as monotherapy in patients with obstructive HCM; ACACIA-HCM, a Phase 3 clinical trial of aficamten in patients with non-obstructive HCM; CEDAR-HCM, a clinical trial of aficamten in a pediatric population with obstructive HCM; and FOREST-HCM, an open-label extension clinical study of aficamten in patients with HCM. About Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy (HCM) is a disease in which the heart muscle (myocardium) becomes abnormally thick (hypertrophied). The thickening of cardiac muscle leads to the inside of the left ventricle becoming smaller and stiffer, and thus the ventricle becomes less able to relax and fill with blood. This ultimately limits the heart’s pumping function, resulting in reduced exercise capacity and symptoms including chest pain, dizziness, shortness of breath, or fainting during physical activity. HCM is the most common monogenic inherited cardiovascular disorder, with approximately 280,000 patients diagnosed, however, there are an estimated 400,000-800,000 additional patients who remain undiagnosed in the U.S.2,3,4 Two-thirds of patients with HCM have obstructive HCM (oHCM), where the thickening of the cardiac muscle leads to left ventricular outflow tract (LVOT) obstruction, while one-third have non-obstructive HCM (nHCM), where blood flow isn’t impacted, but the heart muscle is still thickened. People with HCM are at high risk of also developing cardiovascular complications including atrial fibrillation, stroke and mitral valve disease.5 People with HCM are at risk for potentially fatal ventricular arrhythmias and it is one of the leading causes of sudden cardiac death in younger people or athletes.6 A subset of patients with HCM are at high risk of progressive disease leading to dilated cardiomyopathy and heart failure necessitating cardiac transplantation. About Cytokinetics Cytokinetics is a leading muscle biology specialty biopharmaceutical company focused on discovering, developing and commercializing muscle biology-directed drug candidates as potential treatments for debilitating diseases in which muscle performance is compromised. As a pioneer in muscle and the mechanics of muscle performance, Cytokinetics is intent on meaningfully improving the lives of patients through global access to innovative medicines. Cytokinetics is readying for potential regulatory approvals and commercialization of aficamten, a potential next-in-class cardiac myosin inhibitor, following positive results from SEQUOIA-HCM, the pivotal Phase 3 clinical trial in patients with obstructive hypertrophic cardiomyopathy (HCM). Aficamten is also being evaluated in additional clinical trials enrolling patients with obstructive and non-obstructive HCM. Cytokinetics is also developing omecamtiv mecarbil, a cardiac myosin activator, in patients with heart failure with severely reduced ejection fraction (HFrEF), CK-586, a cardiac myosin inhibitor with a mechanism of action distinct from aficamten, for the potential treatment of heart failure with preserved ejection fraction (HFpEF) and CK-089, a fast skeletal muscle troponin activator with potential therapeutic application to a specific type of muscular dystrophy and other conditions of impaired skeletal muscle function. For additional information about Cytokinetics, visit www.cytokinetics.com and follow us on X, LinkedIn, Facebook and YouTube. Forward-Looking Statements This press release contains forward-looking statements for purposes of the Private Securities Litigation Reform Act of 1995 (the “Act”). Cytokinetics disclaims any intent or obligation to update these forward-looking statements and claims the protection of the Act’s Safe Harbor for forward-looking statements. Examples of such statements include, but are not limited to, statements express or implied relating to the properties, treatment effect or potential benefits of aficamten or any of our other drug candidates or our ability to obtain regulatory approval for aficamten for the treatment of obstructive hypertrophic cardiomyopathy or any other indication from FDA or any other regulatory body in the United States or abroad. Such statements are based on management’s current expectations, but actual results may differ materially due to various risks and uncertainties, including, but not limited to the risks related to Cytokinetics’ business outlines in Cytokinetics’ filings with the Securities and Exchange Commission. Forward-looking statements are not guarantees of future performance, and Cytokinetics’ actual results of operations, financial condition and liquidity, and the development of the industry in which it operates, may differ materially from the forward-looking statements contained in this press release. Any forward-looking statements that Cytokinetics makes in this press release speak only as of the date of this press release. Cytokinetics assumes no obligation to update its forward-looking statements whether as a result of new information, future events or otherwise, after the date of this press release. CYTOKINETICS® and the CYTOKINETICS and C-shaped logo are registered trademarks of Cytokinetics in the U.S. and certain other countries. Contact: Cytokinetics Diane Weiser Senior Vice President, Corporate Affairs (415) 290-7757 References: Source: Cytokinetics, Incorporated

Phase 3Clinical ResultNDABreakthrough TherapyPriority Review

100 Deals associated with Paroxetine Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
-	Paroxetine Hydrochloride	N06AB05	DB00715

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Premenstrual Dysphoric Disorder	United States	Apotex, Inc.	28 Aug 2003
Panic	Japan	GlaxoSmithKline KK	22 Sep 2000
Generalized anxiety disorder	United States	Apotex, Inc.	25 Jun 1997
Stress Disorders, Post-Traumatic	United States	Apotex, Inc.	25 Jun 1997
Depressive Disorder	China	Sino-American Tianjin SmithKline & French Lab., Ltd.	01 Jan 1995
Depressive Disorder, Major	United States	Apotex, Inc.	29 Dec 1992
Obsessive-Compulsive Disorder	United States	Apotex, Inc.	29 Dec 1992
Panic Disorder	United States	Apotex, Inc.	29 Dec 1992
Phobia, Social	United States	Apotex, Inc.	29 Dec 1992

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Anxiety Disorders	Phase 2	Sweden	GSK Plc	01 Nov 2004
Parkinson Disease	Phase 2	United States	GSK Plc	01 Jun 2003
Depressive Disorder, Treatment-Resistant	Clinical	United States	GSK Plc	01 Dec 2003

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05470465 (CTgov)	Phase 1	Hypercarbia	27	Placebo+Oxycodone (Treatment A: Placebo)	lvbccqkqgi(unqryjpxqy) = ugjlknzvjn stpwmshrme (nsozupuxbd, zxwxirhmrm - pqleoelxqp) View more	-	22 May 2025
				Paroxetine+Oxycodone (Treatment B: Paroxetine)	lvbccqkqgi(unqryjpxqy) = adrtdrngxs stpwmshrme (nsozupuxbd, tvtkpmuvlz - tartvkelwv) View more
NCT06065735 (CTgov)	Phase 1	Anxiety Disorders	38	Paroxetine (Participants Who Received Paroxetine 20 mg)	bsfnucvbmm(samadcfiwg) = tiqeqgcqme jiiwehbmop (ppxdmpwvzu, 7.37) View more	-	16 Dec 2024
				Paroxetine (Participants Who Received Paroxetine 40 mg)	bsfnucvbmm(samadcfiwg) = cpjuqzkubs jiiwehbmop (ppxdmpwvzu, 10.82) View more
UEGW2023	Not Applicable	Heartburn	-	Paroxetine 10mg	ouclgvquwk(ypimtqoada) = jzvxzekmti dybbfzcjut (nthedpylhw )	-	15 Oct 2023
				Paroxetine 20mg	ouclgvquwk(ypimtqoada) = hmdnhsxfpq dybbfzcjut (nthedpylhw )
PRRERCT (WCD2023)	Not Applicable	Rosacea \| Erythema	97	Paroxetine 25 mg	qwynulzeyv(kprkxtfbya) = tkigkayywy ctagjhlgjo (jemtogcbbs ) View more	Positive	04 Jul 2023
				Placebo	qwynulzeyv(kprkxtfbya) = egpvioakdk ctagjhlgjo (jemtogcbbs ) View more
NCT04311463 (CTgov)	Phase 1	Anxiety Disorders	38	Paroxetine (Paroxetine 20 mg (Test A))	njxiplpcuq(jkuzfvkiei) = hlqsrccbxb gdamuojgqf (zatzkswais, 5.872) View more	-	20 Jan 2022
				Paroxetine (Paroxetine 20 mg (Reference B))	njxiplpcuq(jkuzfvkiei) = fvjtqbphnk gdamuojgqf (zatzkswais, 6.554) View more
AAN2020	Not Applicable	-	24	Valbenazine 40 mg	qmhlxnyynz(xqigpclcnf) = hbgsbwodzm kpamntzjfl (qfhmcrfjja, 77.1 - 107.8) View more	-	14 Apr 2020
				Valbenazine 40 mg + Paroxetine 20 mg	qmhlxnyynz(xqigpclcnf) = tlgtxddhrn kpamntzjfl (qfhmcrfjja, 157.6 - 229.5) View more
NCT03329573 (CTgov)	Phase 1	Anxiety Disorders	85	GSKT+Paroxetine (Paroxetine 40 mg, GSKT- Fed)	kmoseawdcg(reqequndzi) = ogneznchst wwrtwbypdz (kymjgkrmqj, owjaodaauq - hhnlaejncu) View more	-	19 Aug 2019
				Paroxetine (Paroxetine 40 mg, Mississauga- Fed)	kmoseawdcg(reqequndzi) = hsuoqgljbv wwrtwbypdz (kymjgkrmqj, wmkptmbnse - tgaismixiq) View more
UEGW2018	Not Applicable	Dyspepsia	-	Fluoxetine	cybmxdoagv(gfkwqdgwqe) = kfrfwsetnt alcikfmubt (ipxjndozhl )	-	01 Oct 2018
				Flupenthixol melitracen	cybmxdoagv(gfkwqdgwqe) = hspvzaswwi alcikfmubt (ipxjndozhl )
NCT00246441 (CTgov)	Phase 4	Alcoholism \| Phobia, Social	42	Paroxetine (Paroxetine)	csombkcppz(znloweonpb) = bdrtzkqrff prvbrrgqrh (gqyswzojqa, 14.9) View more	-	27 Sep 2018
				Placebo (Placebo)	csombkcppz(znloweonpb) = wfcybkijbs prvbrrgqrh (gqyswzojqa, 18.5) View more
NCT00420641 (CTgov)	Phase 2	Depressive Disorder, Major	492	Placebo	kiogxgbjoe(xsejpbqxdj) = rqdsbmyask zwxeibaqdf (isipoimhcx, 9.97) View more	-	05 Feb 2018

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

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

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.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis