A Prospective, Single-arm, Phase 4 Study to Evaluate the Course of Serum Transthyretin (TTR) Level With Acoramidis in Adult Patients With Variant or Wild-type Transthyretin Amyloidosis With Cardiomyopathy (ATTR-CM) Previously Treated With Tafamidis

Transthyretin (TTR) is a protein made by the liver that helps transport thyroid hormone and vitamin A in the blood. In some people, this protein breaks down and forms harmful clumps called amyloid. TTR amyloid gets deposited in the heart wall and stops it from pumping blood properly, which may lead to heart failure. The breakage in TTR protein can be age-related (wild-type ATTR-CM), or genetic (variant ATTR-CM).
The study drug, acoramidis, works by attaching itself to the TTR protein, making TTR more stable and less likely to break down and form amyloid (clumps). This helps to slow down the progression of the disease, improve heart function, and increase the TTR levels in the blood. Acoramidis is an approved treatment for wild-type or variant ATTR-CM in Europe and the United States.
Tafamidis is another drug that stabilizes TTR and prevents it from breaking down.
In this study, acoramidis will be studied in participants with ATTR--CM who were previously treated with tafamidis. The main purpose of this study is to assess the change in blood TTR levels after participants are switched from tafamidis to acoramidis. This will be studied to understand if acoramidis causes an increase in blood TTR levels beyond the levels achieved with tafamidis.
For this, the researchers will measure the change in the levels of TTR protein in participants' blood after 6 months of the treatment with acoramidis, or earlier if a participant stops the treatment before reaching that six-month mark.
All participants will continue taking tafamidis during the screening period. In the treatment period of the study, participants will take acoramidis as two tablets twice daily by mouth, for up to 6 months.
At the start of this study, the study doctors will review each participant's medical history and check their overall health. The study doctors will perform electrocardiograms (ECG), and measure blood pressure and heart rate. Researchers will also take blood and urine samples from the participants to measure levels of TTr, NT-proBNP, hs-TnT, hs-CRP, RBP4, eGFR, creatinine, cystatin-C, UACR, and TSH at the start of the study, and at various time points thereafter (during the study) to assess heart, kidney and thyroid function.
There will be a total of 9 study check-ins. Participants will visit the study site twice: at screening and at the end of treatment period. A study nurse will visit the participant's home 6 times, at the start of treatment, Weeks 1, 2, 3 and 4, then again at 3 months. The final check-in will be done by phone.
The study doctors will monitor the health of the participants regularly for any medical problems during follow-up visits. Participants will know the treatment they will receive during the study. Each participant could be in the study for about 8 months.

Start Date13 Feb 2026

Sponsor / Collaborator

Bayer AG

NCT07116473

/ Not yet recruitingPhase 3

A Phase 3, Open-Label, Multicenter, Extension Study of Acoramidis in Patients With Newly Diagnosed Variant Transthyretin Amyloid Cardiomyopathy (ACT-EARLY OLE)

The AG10-504 study is an open-label extension study of acoramidis in participants with newly diagnosed transthyretin amyloid cardiomyopathy (ATTR-CM) or both ATTR-CM and transthyretin amyloid polyneuropathy (ATTR-PN).

Start Date01 Nov 2025

Sponsor / Collaborator

Eidos Therapeutics, Inc.

NCT07235462

/ RecruitingNot Applicable

ACO-REAL - A Non-interventional Study Providing Insights Into the Use of Acoramidis in Patients With ATTR Amyloidosis With Cardiomyopathy (ATTR-CM) in Routine Clinical Practice

Transthyretin Amyloid Cardiomyopathy (ATTR-CM) is a serious and life-threatening condition where a protein called transthyretin (TTR) misfolds and builds up as amyloid fibrils in the heart muscle. This buildup causes the heart to become stiff, leading to restrictive cardiomyopathy and progressive heart failure. There are two forms of ATTR-CM: a hereditary or 'variant' form (vATTR-CM) caused by a gene mutation, and a 'wild-type' form (wtATTR-CM) which is associated with aging. Because its symptoms can be similar to other heart conditions, ATTR-CM is often diagnosed late. However, recent advances in medical imaging are helping doctors to identify the disease earlier. Acoramidis is a new medication designed to treat ATTR-CM. It works by stabilizing the TTR protein, preventing it from misfolding and forming the harmful amyloid deposits. Acoramidis has been shown to be effective and safe in a major clinical trial (the ATTRibute-CM study), which led to its approval for use in both the United States and Europe. While clinical trials provide valuable information, data on how a new medicine performs in everyday clinical practice is also very important. This type of information is called real-world evidence. Currently, there is limited real-world information about the use of acoramidis. This study, called ACO-REAL, is an observational study, which means researchers will observe patients who are receiving acoramidis as part of their normal clinical care, without introducing any experimental interventions. The study will take place in approximately 20 European countries and aims to enroll up to 2,000 adults who have been diagnosed with either wild-type or variant ATTR-CM and are starting treatment with acoramidis. This includes patients who have not been treated for ATTR-CM before, as well as those who have been treated with other therapies. The main goals of the study are to understand the characteristics of patients being treated with acoramidis and to document how the treatment is used in routine medical practice. The study will also collect information on the safety of acoramidis. Furthermore, researchers will assess how the treatment affects patients' heart function, their functional capacity (such as their ability to walk), their overall health status, and their quality of life. The study will also track how often patients need to use healthcare resources like hospitals or emergency rooms. This information will help to improve the understanding and management of ATTR-CM in a real-world setting, ultimately aiming to optimize care for patients with this progressive disease.

Start Date29 Oct 2025

Sponsor / Collaborator

Bayer AG

100 Clinical Results associated with Acoramidis

100 Translational Medicine associated with Acoramidis

100 Patents (Medical) associated with Acoramidis

Literatures (Medical) associated with Acoramidis

01 Jun 2026·CURRENT THERAPEUTIC RESEARCH-CLINICAL AND EXPERIMENTAL

Understanding Pharmacokinetic-Drug Interactions With Drugs Approved by the US Food and Drug Administration in 2024 to Better Manage the Risk of Drug Interactions With Concomitant Medications: A Review of Clinical Data From New Drug Applications

Review

Author: Owens, Katie ; Argon, Sophie ; Yu, Jingjing ; Ragueneau-Majlessi, Isabelle ; Wang, Yan

Objective:

This analysis aimed to provide a mechanistic understanding and an evaluation of the clinical relevance of pharmacokinetic drug-drug interactions (DDIs) associated with drugs approved by the Food and Drug Administration in 2024.

Methods:

Drug metabolism, transport, and absorption-based DDI data available in New Drug Applications (NDAs) of small molecular drugs approved (n = 34) was analyzed. The mechanism and clinical outcome of these interactions were characterized based on in vitro, in silico, and clinical data.

Results:

As objects, 11 drugs were identified as clinical substrates. Of these, 7 drugs were substrates of CYP3A, 3 of CYP2C9, one of CYP1A2, and one of CYP2C8, including the sensitive substrates vanzacaftor (CYP3A) and vorasidenib (CYP1A2). As precipitants, 6 drugs (acoramidis, cefepime/enmetazobactam, givinostat, lazertinib, mavorixafor, and resmetirom) were clinical inhibitors of CYP enzymes (2C8, 2C9, 2D6, 2E1, and 3A), with mavorixafor being a CYP2D6 strong inhibitor. Two drugs (elafibranor and tovorafenib) showed weak induction of CYP3A. Regarding transporter data, 3 drugs were substrates of transporters, including seladelpar (BCRP and OAT3), sulopenem (OAT3), and vadadustat (OAT1/3), and 8 drugs (arimoclomol, danicopan, givinostat, lazertinib, mavorixafor, resmetirom, vadadustat, and vazacaftor/tezacaftor/deutivacaftor) were inhibitors of transporters. All clinical DDIs with AUC changes ≥ 2-fold triggered labeling recommendations. Several DDIs with an AUC change <2 also had labeling recommendations, pertaining most often to the concomitant use of drugs with a narrow therapeutic index.

Conclusions:

Mechanistic DDI insights from newly approved therapies can be extrapolated to inform the management of commonly co-administered drugs, supporting a safer and more effective use of new drug products in the context of polypharmacy.

01 May 2026·INTERNATIONAL JOURNAL OF CARDIOLOGY

Hidden overlap between heart failure with preserved ejection fraction and transthyretin amyloid cardiomyopathy: Why it matters and how to avoid missing it

Review

Author: Tanaka, Hidekazu

Transthyretin cardiac amyloidosis (ATTR-CM) is increasingly recognized as a treatable cause of heart failure, while heart failure with preserved ejection fraction (HFpEF) has become one of the most common and heterogeneous heart failure syndromes worldwide. Growing evidence shows that a substantial proportion of patients diagnosed with HFpEF actually harbor unrecognized ATTR-CM. Missing this diagnosis may limit the effectiveness of HFpEF therapies and delay initiation of disease-modifying treatment. Screening studies consistently demonstrate that ATTR-CM represents an important subset of HFpEF, particularly in individuals with increased left ventricular wall thickness, elevated natriuretic peptides, or unexplained conduction abnormalities. Although HFpEF and ATTR-CM share significant clinical overlap, several reproducible red-flags such as discordance between electrocardiographic voltages and wall thickness, pseudo infarct patterns, carpal tunnel syndrome, progressive troponin elevation, and apical sparing on strain imaging provide important early diagnostic clues. These features, together with emerging scoring tools, help identify patients at increased risk. In addition, bone scintigraphy has transformed the diagnostic pathway by enabling noninvasive confirmation of ATTR-CM in the absence of monoclonal protein. As disease-modifying agents such as tafamidis, acoramidis, and vutrisiran become widely available, early recognition is increasingly essential. This review synthesizes epidemiologic data on the prevalence of ATTR-CM among HFpEF cohorts, highlights key diagnostic pitfalls, and outlines practical strategies to facilitate timely detection. The aim is to support clinicians managing HFpEF by proposing a pragmatic, red-flag based screening framework that reduces missed diagnoses and enables appropriate initiation of disease-modifying therapy.

01 Apr 2026·CURRENT PROBLEMS IN CARDIOLOGY

Impact of disease-modifying therapies on imaging parameters in cardiac amyloidosis: A systematic review and meta-analysis

Review

Author: Zervas, Georgios ; Briasoulis, Alexandros ; Patras, Raphael ; Androulakis, Emmanuil ; Tepetes, Nikolaos ; Georgiopoulos, Georgios ; Kastritis, Efstathios ; Lama, Niki ; Kourek, Christos ; Stamatelopoulos, Kimon ; Theodorakakou, Foteini

Transthyretin-mediated (ATTR) and immunoglobulin light-chain (AL) cardiac amyloidosis causes progressive myocardial dysfunction and poor prognosis. Disease-specific therapies in ATTR and anti-clonal therapies in AL cardiac amyloidosis may modify disease, but treatment-induced changes in prognostic cardiac imaging markers remain incompletely defined. We systematically searched PubMed/MEDLINE, Scopus, CINAHL, Web of Science, and EMBASE for studies reporting treatment-associated changes in global longitudinal strain (GLS), left ventricular (LV) wall thickness, and extracellular volume (ECV) assessed by echocardiography or cardiac magnetic resonance. Random-effects meta-analyses pooled mean changes. Seventeen studies met inclusion criteria. In ATTR cardiac amyloidosis, therapy with silencers or RNA-depleting agents was associated with improved GLS (pooled mean difference [MD] -0.97 %, 95 % CI -1.27 to -0.68) and reduced LV wall thickness (MD -0.72 mm, 95 % CI -1.26 to -0.17) versus no therapy, while ECV showed no significant change (MD -1.93 %, 95 % CI -15.27 to 11.41). In AL amyloidosis, complete hematologic response was linked to greater improvement than non-response in GLS (MD -1.19 %, 95 % CI -2.20 to -0.17) and LV wall thickness (MD -0.87 mm, 95 % CI -1.31 to -0.43). NMA in ATTR cardiac amyloidosis showed that patisiran (MD -1.04 %, 95 % CI -1.56 to -0.52), tafamidis (-0.91 %, -1.40 to -0.41), and vutrisiran (-0.90 %, -1.75 to -0.05) improved GLS versus placebo, compared to acoramidis. Disease-directed therapy in ATTR and hematologic response in AL cardiac amyloidosis are associated with preservation or improvement of GLS and LV wall thickness, supporting their use as surrogate endpoints for treatment monitoring.

199

News (Medical) associated with Acoramidis

31 Mar 2026

·allsci.com

BridgeBio’s acoramidis shows sustained mortality reduction in 54-month ATTR-CM extension study

BridgeBio Pharma (Nasdaq: BBIO) reported 54-month open-label extension data for acoramidis (Attruby) in ATTR-CM associated with a 44.7% reduction in all-cause mortality and 49.3% reduction in cardiovascular mortality versus patients who had received placebo before crossing over to active treatment, with both results reaching p<0.0001. The ATTRibute-CM open-label extension is an active, unblinded follow-on study enrolling adults with transthyretin amyloid cardiomyopathy who completed the parent randomized controlled trial, comparing outcomes in patients who received continuous acoramidis against those who transitioned from placebo. At Month 54, the mortality separation between the continuous-treatment and placebo-crossover groups was statistically robust on both endpoints. Acoramidis also attenuated the rise in NT-proBNP — a marker of cardiac wall stress and a surrogate for disease progression — to a degree the company characterized as exceeding what has been observed with other disease-modifying treatments in ATTR-CM. Heart failure-related quality of life, measured by the Kansas City Cardiomyopathy Questionnaire Overall Summary score, was stabilized and maintained through Month 54 in patients who received early and continuous treatment. A secondary analysis showed that an early increase in serum transthyretin at Day 28 was associated with slower KCCQ-OS decline at Month 30, suggesting the pharmacodynamic response predicts longer-term functional benefit. While continuous acoramidis treatment was associated with statistically significant reductions in all-cause and cardiovascular mortality versus patients who crossed over from placebo, because the extension was open-label and non-randomized, the findings should be interpreted as supportive long-term durability data rather than evidence of superiority versus other approved ATTR-CM therapies. The safety profile remained consistent with the parent trial. Diarrhea occurred in 11.6% of acoramidis-treated patients versus 7.6% on placebo, and upper abdominal pain in 5.5% versus 1.4%; both were predominantly mild and resolved without drug discontinuation. Discontinuation rates due to adverse events were similar between groups (9.3% versus 8.5%). Developed by BridgeBio Pharma and licensed from Stanford University, acoramidis is a second-generation oral transthyretin (TTR) stabilizer approved in late 2024 (USA) and early 2025 (EU, Japan) for transthyretin amyloid cardiomyopathy (ATTR-CM). Designed to mimic a protective genetic variant, it offers near-complete stabilization (around 90%) of the TTR protein, a figure that distinguishes it mechanistically from tafamidis (Vyndaqel/Vyndamax), the incumbent standard of care, which achieves approximately 60% stabilization in vitro. Whether that pharmacological difference translates into a clinically meaningful outcome advantage over tafamidis has not been established in a direct head-to-head trial; cross-trial comparisons are limited by differences in patient populations, trial design, and follow-up duration. A comparative imaging study of tafamidis versus acoramidis is currently recruiting, and a Phase IV switch study is listed as not yet recruiting. The competitive landscape in ATTR-CM has shifted since acoramidis received FDA approval in November 2024. Alnylam’s vutrisiran (Amvuttra), an RNA interference therapy that silences hepatic TTR production rather than stabilizing the protein, received FDA approval for ATTR-CM in March 2025, introducing a mechanistically distinct option with quarterly subcutaneous dosing, following a Phase III trial in ATTR-CM. The entry of an RNAi agent into the same patient population creates a two-axis competitive dynamic: acoramidis competes with tafamidis on potency within the oral stabilizer class, and with vutrisiran on route of administration and mechanism. A real-world survey presented alongside the OLE data at the American College of Cardiology meeting found that physicians were unsatisfied with treatment in more than half of patients currently prescribed therapy, and that more than one-third of patients received no treatment at all — with oral therapy the most preferred format among patients. The OLE data were presented as a late-breaking oral at the ACC Annual Scientific Sessions and simultaneously published in JAMA Cardiology, lending the readout additional visibility in the cardiology community. The open-label, non-randomized design of the extension study introduces limitations that are standard for this type of analysis: the comparator group is patients who started treatment later rather than a concurrent control arm, and unblinding may influence both patient behavior and clinical management decisions. The patient population size for the OLE was not disclosed in the press release. BridgeBio stated that additional Attruby data are planned for future medical meetings. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

Clinical ResultPhase 3Drug Approval

24 Mar 2026

·endpoints.news

UK biotech co-founded by Nobel laureate secures $86M for antibody program

A British biotech based in Cambridge, England, raised $86 million to advance an antibody drug designed to deplete protein deposits in people with amyloidosis. The company, called Immutrin, was co-founded by Gregory Winter. He won the 2018 Nobel Prize in Chemistry along with two other scientists for pioneering a lab technique known as “phage display” to develop new proteins, including therapeutic antibodies. Academics Mark Pepys and Daniel Christ were also involved in founding Immutrin. The biotech’s approach is largely based on Pepys’ work, but Winter was “instrumental in terms of precisely engineering the antibody to the specifications that we needed,” Immutrin CEO Mihriban Tuna told Endpoints News. That unnamed antibody is now in preclinical development for a form of amyloidosis called ATTR cardiomyopathy, which affects the heart. It targets the disease in a “very unique” way compared to available treatments like Pfizer’s Vyndaqel and BridgeBio’s Attruby, Tuna said. Vyndaqel and Attruby stop the disease getting worse by preventing the production of further amyloid fibrils. By contrast, Immutrin’s candidate is designed to selectively bind to fibrils that have already formed in the heart, removing them by inducing a targeted immune response. “It actually offers the possibility for reversing disease, rather than simply slowing down progression,” Tuna said. The two approaches could even be used in combination, she said. Immutrin is working to start its proof-of-concept trial “as soon as possible.” While the biotech is currently focused on ATTR cardiomyopathy, it could also address other forms of amyloidosis in the future, including rarer types for which there are no approved treatments, Tuna said. Frazier Life Sciences led the Series A funding round, and F-Prime Capital, Qiming Venture Partners and SR One also invested. The company’s founding investors, Cambridge Innovation Capital and Cambridge Enterprise Ventures, chipped in as well.

ADC

24 Mar 2026

·www.biopharmadive.com

Immutrin raises $87M to advance drug for progressive heart disease

Immutrin, a U.K.-based biotechnology company developing next-generation antibody therapies, has raised $87 million in a Series A funding round to advance its lead candidate for a genetic, progressive heart disease.Immutrin said Tuesday the money will be used to get the companys lead candidate through an early-stage trial for transthyretin amyloid cardiomyopathy, or ATTR-CM, a disease where a toxic buildup of transport protein can result in heart failure and death. It's the cardiac manifestation a condition known as transthyretin amyloidosis, which can also affect nerves and impair certain body systems. ATTR-CM primarily affects the heart, causing symptoms such as shortness of breath, swelling in the legs and an irregular heartbeat.Pfizer developed the first approved drug, tafamidis, to treat the cardiac form of transthyretin amyloidosis. Sold as Vyndaqel, Vyndamax and Vynmac, it became a fast-growing product that spurred development from other drugmakers who saw ATTR-CM as a lucrative market.BridgeBio and Alnylam Pharmaceuticals have become the top competitors after Pfizer. BridgeBios Attruby was approved in 2024, while Alnylams Amvuttra gained cleared by the Food and Drug Administration last year. Both medicines quickly gained traction, with Amvuttra leading Alnylam into profitability.Other companies are still trying to secure a spot on the market. In late 2023, the FDA approved AstraZeneca and Ionis Pharmaceuticals Wainua as a treatment for a form of transthyretin amyloidosis that affects the peripheral and autonomic nervous system. The medicine is currently in Phase 3 testing for ATTR-CM and has received a Fast Track designation to speed its review.Intellia Therapeutics, meanwhile, is developing a candidate using gene-editing technology. However, the company faced a setback last May after a safety signal was identified in an ongoing late-stage study.Immuntrin believes theres a place for its lead candidate as well. The antibody drug is designed to get the immune system to help remove accumulated transthyretin deposits in body tissues, which is different than currently marketed therapies. Attruby and tafamidis are transthyretin stabilizers that work to prevent these proteins from misfolding, while Amvuttra uses RNA interference to silence the misfolded proteins by suppressing their production.Immuntri said its candidate may also have the potential to treat other types of conditions caused by amyloidosis, including uncommon ones.The Series A round was led by Frazier Life Sciences, and had participation from Qiming Venture Partners, F-Prime, SR One and Immuntris founding investors Cambridge Enterprise Ventures and Cambridge Innovation Capital.As part of the funding disclosure, Immuntri announced its board of directors will be adding Michael Anstey, partner at Cambridge Innovation Capital, James Topper, managing partner at Frazier Life Sciences, Nihal Sinha, partner at F-Prime and Alex Sinclair-Wilson, principal at Qiming Venture Partners. '

Drug ApprovalPhase 3Fast Track

100 Deals associated with Acoramidis

External Link

KEGG	Wiki	ATC	Drug Bank
D11972	-	-	-

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Amyloidosis, Hereditary, Transthyretin-Related	European Union	Bayer AG	10 Feb 2025
Amyloidosis, Hereditary, Transthyretin-Related	Iceland	Bayer AG	10 Feb 2025
Amyloidosis, Hereditary, Transthyretin-Related	Liechtenstein	Bayer AG	10 Feb 2025
Amyloidosis, Hereditary, Transthyretin-Related	Norway	Bayer AG	10 Feb 2025
Transthyretin Amyloid Cardiomyopathy	United States	BridgeBio Pharma, Inc.	22 Nov 2024

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Polyneuropathies	Phase 3	United States	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Japan	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Argentina	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Australia	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Belgium	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Brazil	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Canada	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Denmark	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	France	Eidos Therapeutics, Inc.	12 May 2025
Polyneuropathies	Phase 3	Germany	Eidos Therapeutics, Inc.	12 May 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03860935 (ATTRibute-CM OLE, GlobeNewswire) Manual	Phase 3	Transthyretin Amyloid Cardiomyopathy	286	acoramidis	ptbmizmcsp(vrwrsmqams): Difference (%) = -44 View more	Positive	30 Aug 2025
				Placebo
NCT03860935 (ATTRibute-CM, Pubmed \| Am J Cardiovasc Drugs)	Phase 3	Transthyretin Amyloid Cardiomyopathy	632	Acoramidis hydrochloride	ajqqumflzu(vbcgyplgoi) = cqpaifpcqb zizamotopt (dmtigpurhk ) View more	Positive	01 Aug 2025
NCT03860935 (ATTRibute-CM, Pubmed \| J Am Coll Cardiol)	Phase 3	Transthyretin Amyloid Cardiomyopathy sTTR levels	557	Acoramidis	iohlzzkcst(nvimoadlgl) = was associated with reduced ACM in univariate analysis (HR: 0.96 per 1 mg/dL increase in early ΔTTR; 95% CI: 0.93-0.98; P = 0.002). In the multivariate analysis, after adjusting for TTR variant status, baseline New York Heart Association functional class, baseline National Amyloidosis Centre stage, and baseline sTTR level, early ΔTTR remained independently associated with reduced ACM (P < 0.001). hpodaodexc (bhwvuvgwhq ) View more	Positive	01 May 2025
NCT03860935 (ATTRibute-CM, Pubmed \| J Am Coll Cardiol)	Phase 3	Transthyretin Amyloid Cardiomyopathy \| Senile cardiac amyloidosis N-terminal pro-B-type natriuretic peptide level	632	Acoramidis hydrochloride 800 mg twice daily	aekcgtrgzx(cclnurpnci): relative risk ratio = 50 (95% CI, 0.36 - 0.7), P-Value = < 0.0001 View more	Positive	01 Mar 2025
				Placebo
NCT04622046 (CTgov)	Phase 3	Transthyretin Amyloid Cardiomyopathy	25	ALXN2060	zdddynramr(pxwaupwacz) = tirdcnoabv kkvsmfyiny (gfsxcrgbmg, 9.182) View more	-	16 Dec 2024
NCT03860935 (FDA_CDER) Manual	Phase 3	Transthyretin Amyloid Cardiomyopathy	611	ATTRUBY 712 mgATTRUBY 712 mg	gsvdgcnezh(drclqytobr): P-Value = 0.018 View more	Positive	22 Nov 2024
				Placebo
NCT03860935 (ATTRibute-CM, Company_Website) Manual	Phase 3	Transthyretin Amyloid Cardiomyopathy	389	Acoramidis	adgopxgueh(pyfkyxjjhu) = dsfroetryw huowwjxpey (pdmqsucnvk ) View more	Positive	18 Nov 2024
				Placebo	-
NCT03860935 (ATTRibute-CM, GlobeNewswire \| PipelineReview) Manual	Phase 3	Transthyretin Amyloid Cardiomyopathy	-	Acoramidis	yqphhmrsxs(epluoramuu) = vgbwpzmgfb fxaczpiojy (ussajjzzht )	Positive	27 Sep 2024
				Placebo	-
NCT03860935 (ATTRibute-CM, ESC2024)	Phase 3	Transthyretin Amyloid Cardiomyopathy serum TTR levels	611	Acoramidis	thewdfprxt(reogcfsxbs) = jfbboulinn cdoiyfqntf (wjueqexnjx )	Positive	30 Aug 2024
				Tafamidis	thewdfprxt(reogcfsxbs) = bzfnwbzlsf cdoiyfqntf (wjueqexnjx, 0.4 (4.92))
NCT03860935 (ATTRibute-CM OLE \| ATTRibute-CM, CTgov)	Phase 3	Transthyretin Amyloid Cardiomyopathy \| Senile cardiac amyloidosis	632	acoramidis (Acoramidis HCl 800 mg)	rrhugtarlx = qezlhiboxl sdubesjeoe (blvcuaeixq, wcitoydvun - zneuznthbx) View more	-	27 Jun 2024
				Placebo Oral Tablet (Placebo)	rrhugtarlx = pjeyxifgqp sdubesjeoe (blvcuaeixq, txdnpuwfzg - hqxqcpjiqi) View more

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