A Phase II, Randomised, Double Blind, Placebo-controlled Study of the Pharmacokinetics, Pharmacodynamic Effects, and Safety, of Oral FT011 in Participants With Diffuse Systemic Sclerosis

FT011 is an anti-fibrotic drug that is being tested as a treatment for scleroderma. This study is being conducted to see what the body does to the drug (pharmacokinetics), and what the drug does to the body (pharmacodynamics).

开始日期2021-07-19

申办/合作机构

Certa Therapeutics Pty Ltd.初创企业

ACTRN12618000033246 / Completed临床1期

A double-blind, placebo-controlled, randomised trial to determine the ocular pharmacokinetics and safety of oral FT011 in patients with glaucoma.

开始日期2019-05-13

申办/合作机构

OccuRx Pty Ltd初创企业

ACTRN12613000386730 / Completed临床1期

A Phase I, double blind, randomised, placebo-controlled, dose-escalating study of the safety, tolerability, food effect and pharmacokinetics of single and repeat doses of FT011 administered orally to healthy volunteers and patients with diabetic nephropathy associated with Type 2 diabetes

开始日期2013-05-20

申办/合作机构

Fibrotech Therapeutics Pty Ltd.

100 项与 Asengeprast 相关的临床结果

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100 项与 Asengeprast 相关的转化医学

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100 项与 Asengeprast 相关的专利（医药）

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项与 Asengeprast 相关的文献（医药）

2013-09-01·International journal of cardiology2区 · 医学

A new anti-fibrotic drug attenuates cardiac remodeling and systolic dysfunction following experimental myocardial infarction

2区 · 医学

Article

作者: Steven C Zammit ; Amanda Jane Edgley ; Richard E Gilbert ; Alison Cox ; Spencer John Williams ; Maros Elsik ; Andrew Richard Kompa ; Henry Krum ; Christina Yr Tan ; Bing Hui Wang ; Darren J Kelly ; Fay Lin Khong ; Yuan Zhang ; David I Stapleton

BACKGROUND:

Pathological deposition of extracellular matrix in the non-infarct zone (NIZ) of the ventricle post myocardial infarction (MI) is a key contributor to cardiac remodeling and heart failure. FT011, a novel antifibrotic compound, was evaluated for its efficacy in neonatal cardiac fibroblasts (NCF) and in an experimental MI model.

METHODS AND RESULTS:

Collagen synthesis in NCF was determined by (3)H-proline incorporation following stimulation with TGF-β or angiotensin II (Ang II). FT011 inhibited collagen synthesis to both agents in a dose dependent manner. In vivo, Sprague Dawley rats underwent left anterior descending coronary artery ligation or sham surgery and were randomized one week later to receive either FT011 (200mg/kg/day) or vehicle for a further 4 weeks. Echocardiography and cardiac catheterization were performed, and tissues were collected for histological analysis of collagen, myocyte hypertrophy, interstitial macrophage accumulation and Smad2 phosphorylation. mRNA expression of collagens I and III and TGF-β was measured using in situ hybridization and RT-PCR, respectively. FT011 treatment was associated with improved cardiac function (increased ejection fraction, fraction shortening and preload recruitable stroke work) and myocardial remodeling (reduced left ventricular diameter and volume at both end diastolic and systolic) compared with vehicle treatment. FT011 significantly reduced collagen matrix deposition, myocyte hypertrophy and interstitial macrophage infiltration, and mRNA expression of collagens I and III in NIZ compared with vehicle treatment.

CONCLUSION:

Anti-fibrotic therapy with FT011 in MI rats attenuated fibrosis and preserved systolic function.

2013-03-01·Diabetologia1区 · 医学

Attenuation of Armanni–Ebstein lesions in a rat model of diabetes by a new anti-fibrotic, anti-inflammatory agent, FT011

1区 · 医学

Article

作者: X. Lau ; Y. Zhang ; D. J. Kelly ; D. I. Stapleton

AIMS/HYPOTHESIS:

A key morphological feature of diabetic nephropathy is the accumulation and deposition of glycogen in renal tubular cells, known as Armanni-Ebstein lesions. While this observation has been consistently reported for many years, the molecular basis of these lesions remains unclear.

METHODS:

Using biochemical and histochemical methods, we measured glycogen concentration, glycogen synthase and glycogen phosphorylase enzyme activities, and mRNA expression and protein levels of glycogenin in kidney lysates from control and transgenic (mRen-2)27 rat models of diabetes that had been treated with and without a new anti-fibrotic agent, FT011.

RESULTS:

Diabetic nephropathy was associated with increased glycogen content, increased glycogen synthase activity and decreased glycogen phosphorylase activity. Glycogenin, the key protein responsible for initiating the synthesis of each glycogen particle, had very high levels in the diabetic kidney together with increased mRNA expression compared with control kidneys. Treatment with FT011 did not change glycogen synthase or glycogen phosphorylase enzyme activities but prevented both glycogenin mRNA synthesis and accumulation of Armanni-Ebstein lesions in the diabetic kidney.

CONCLUSIONS/INTERPRETATION:

Armanni-Ebstein lesions found in diabetic nephropathy are due to aberrant glycogenin protein levels and mRNA expression, providing an explanation for the increased glycogen concentration found within the diabetic kidney. FT011 treatment in diabetic rats reduced glycogenin levels and, subsequently, renal glycogen concentration.

2012-05-01·European journal of heart failure1区 · 医学

FT011, a new anti‐fibrotic drug, attenuates fibrosis and chronic heart failure in experimental diabetic cardiomyopathy

1区 · 医学

Article

作者: Kelly, Darren J. ; Wang, Bing ; Zhang, Yuan ; Stapleton, David I. ; Cox, Alison J. ; Gilbert, Richard E. ; Williams, Spencer J. ; Krum, Henry ; Zammit, Steven C. ; Powell, Andrew K. ; Kompa, Andrew R. ; Edgley, Amanda J.

Aims:

Cardiac remodelling in diabetes includes pathological accumulation of extracellular matrix and myocyte hypertrophy that contribute to heart dysfunction. Attenuation of remodelling represents a potential therapeutic target. We tested this hypothesis using a new anti‐fibrotic drug, FT011 (Fibrotech Therapeutics Pty Ltd), on diabetic Ren‐2 rats, a model which replicates many of the structural and functional manifestations of diabetic cardiomyopathy in humans.

Methods and results:

Homozygous Ren‐2 rats were randomized to receive streptozotocin or vehicle then further randomized to FT011 (200 mg/kg/day) or vehicle treatment for 6 weeks. Prior to tissue collection, cardiac function was assessed via echocardiography and cardiac catheterization. Total collagen deposition and cardiomyocyte hypertrophy were assessed by picrosirius red and haematoxylin and eosin staining, respectively. Macrophage interstitial infiltration and type I and III collagen were quantitated by immunostaining. Without affecting blood pressure or hyperglycaemia, treatment of diabetic rats with FT011 significantly attenuated interstitial fibrosis (total collagen, 5.09 ±1.28 vs, 2.42 ±0.43%/area; type I collagen, 4.09 ±1.16 vs. 1.42 ±0.38%/area; type III collagen, 1.52 ±0.33 vs. 0.71 ±0.14 %/area; P < 0.05), cardiomyocyte hypertrophy (882 ±38 vs. 659 ±28 µm2; P < 0.05), and interstitial macrophage influx (66 ±5.3 vs, 44 ±7.9 number/section; P < 0.05). Cardiac myopathic dilatation was normalized, as evidenced by reduced left ventricular inner diameter at diastole (0.642 ±0.016 vs. 0.577 ±0.024 cm), increased ejection fraction (75 ±1.1 vs. 83 ±1.2%) and preload recruitable stroke work relationship (44 ±6.7 vs. 77 ±6.3 slope‐mmHg; P < 0.05), and reduced end‐diastolic pressure–volume relationship (0.059 ±0.011 vs. 0.02 ±0.003 slope‐mmHg/μL; P < 0.05).

Conclusions:

A direct anti‐fibrotic agent, FT011, attenuates cardiac remodelling and dysfunction in experimental diabetic cardiomyopathy. This represents a novel therapy for the treatment of diabetic cardiomyopathy associated with cardiac fibrosis and hypertrophy.

项与 Asengeprast 相关的新闻（医药）

2024-12-19

·GlobeNewswire-Health Care

Certa Therapeutics Expands GPR68 Platform through Acquisition of OccuRx

Strengthened Pipeline Targets Multiple Fibrotic DiseasesMELBOURNE, Australia, Dec. 19, 2024 (GLOBE NEWSWIRE) -- Certa Therapeutics (Certa), a biotechnology company developing innovative precision therapies for patients with fibrotic diseases, today announces the acquisition of OccuRx, a Melbourne-based biotechnology company with highly complementary assets, resources and expertise, and a shared focus on targeting GPR68, a master switch of fibrosis. The acquisition combines the assets and capabilities of two companies founded by a leader in the GPR68 field, Professor Darren Kelly, consolidating a pipeline that now includes two Phase 2 and one Phase 1 clinical candidates. Building on Professor Kelly’s pioneering research into inhibitors of GPR68 and benefiting from years of further development within biotechnology and major pharma companies, Certa’s pipeline aims to tackle fibrotic diseases upstream of other targeted biological pathways. Certa’s lead programme is asengeprast (FT011) a novel, first-in-class oral therapy for the treatment of chronic fibrosis in multiple organs, which has shown favourable efficacy, safety and pharmacokinetics in patients with systemic sclerosis (scleroderma or SSc). Post the acquisition, Certa’s pipeline will include the additional asset OCX063 from OccuRx which has successfully completed a Phase 1 clinical trial and is in development for focal segmental glomerulosclerosis (FSGS), a rare disease characterized by fibrosis developing in the kidney glomerulus. In addition, Certa also has CTA382, a second-generation compound with the same chemical backbone as Asengeprast, that is under development to treat chronic kidney disease and a third-generation series of pre-clinical GPR68 antagonists, based on a different chemical backbone. Assets from this series are being developed for other fibrotic conditions and wider therapeutic indications. Professor Darren Kelly, Certa Therapeutics’ CEO and founder, said, “Fibrotic diseases are an area of significant unmet need, responsible for an estimated 45% of all deaths globally and representing a $15 billion market. We believe GPR68 is a critical ‘master switch’ of fibrosis and through this acquisition we have brought together a unique pipeline and a passionate, experienced team which is uniquely equipped to drive its development. We look forward to rapidly advancing our programs and, ultimately, developing new safe, effective precision therapies for patients.” Asengeprast has its genesis in Fibrotech, which was sold to Shire in 2014. When Shire was then acquired by Takeda in 2018, Brandon Capital Partners and Uniseed had an opportunity to reinvest in the asengeprast clinical program by forming Certa Therapeutics, and to develop GPR68-targeting ophthalmology assets by forming OccuRx. The two companies have raised $30m (AU$44.5m) over the past six years to advance these assets. Certa will now seek to raise a series B to continue the clinical development of its pipeline and expand its operations. Dr Chris Nave, chair of Certa Therapeutics and Managing Partner of lead investor Brandon Capital, said, "Bringing together the assets and expertise of Certa Therapeutics and OccuRx under one company creates a powerful platform to advance transformative therapies for fibrotic diseases. This consolidation reinforces Certa’s leadership in the GPR68 field and its commitment to developing innovative treatments with a promising clinical-stage pipeline of GPR68 antagonists.” For further information please contact Media – AustraliaKirrily Davis, E: kdavis@bcpvc.com M: +61 (0)401 220228 Media - InternationalSue Charles, Charles Consultants E: sue.charles@charles-consultants.com M: +44 (0)7968 726585 About Certa TherapeuticsCerta Therapeutics is a clinical-stage biotechnology company pioneering innovative precision therapies for the treatment of fibrotic diseases—an area of significant unmet need, responsible for an estimated 45% of all deaths globally and representing a $15 billion market. Certa’s platform targets a critical 'master switch' of fibrosis, GPR68 (a defined G protein-coupled receptor (GPCR)), with a pipeline of inhibitors for various fibrotic indications. Asengeprast (FT011), the company’s lead program, is being developed as a novel, first-in-class oral therapy for systemic sclerosis (scleroderma, SSc) and has successfully completed a multi-national, phase II clinical trial. Scleroderma is a potentially-life threatening autoimmune disorder with the highest mortality rate among rheumatic diseases. The FDA has granted asengeprast (FT011) Orphan Drug Designation and Fast Track status for SSc. Certa's pipeline includes further programs targeting major indications such as chronic kidney disease, focal segmental glomerulosclerosis, diabetic nephropathy, and other chronic fibrotic conditions. Based in Melbourne, Australia, Certa is supported by venture investors Brandon Capital and Uniseed. More information at https://certatherapeutics.com/ Follow us on LinkedIn: https://www.linkedin.com/company/certa-therapeutics/

临床1期快速通道并购孤儿药临床2期

2024-09-19

·CPHI制药在线

浅谈系统性硬化病治疗进展，在研疗法作用靶点、药物类型多样

关注并星标CPHI制药在线系统性硬化病（SSc），又称硬皮病，是一种以局限性或弥漫性皮肤及内脏器官纤维化或硬化为特征的自身免疫性结缔组织病，2018年5月被列入中国第一批罕见病目录。SSc常累及全身多系统，包括胃肠道、心脏、肺、肾等脏器，其中肺部受累是SSc是常见且严重的内脏损害之一，主要表现为肺间质病变（ILD）和肺动脉高压（PAH），这两者占SSc相关死亡原因的60%。根据皮肤受累范围及临床特点，SSc可分为四型：局限皮肤型SSc、弥漫皮肤型SSc、重叠综合征和无皮肤硬化型SSc。流行病学数据显示：SSc的全球总患病率为17.6/10万，发病高峰年龄在 45~65岁，女性发病率高于男性，但男性SSc患者往往病情较重，更易出现弥漫性皮肤病变、指端溃疡和肺动脉高压（PAH），预后相对较差。 SSc治疗现状 SSc发病机制复杂，包括自身免疫学说、血管病学说和胶原合成异常学说等。但由于病因未明，SSc长期以来缺乏有效的治疗手段。临床上主要通过免疫药物及一些对症治疗来控制疾病进展，环磷酰胺、甲氨蝶呤、长春新碱等免疫抑制剂抑制来免疫系统的异常反应，减轻炎症和纤维化等病理过程。硫唑嘌呤等免疫调节剂调节免疫系统的功能，减轻自身免疫反应。此外，临床上还使用非甾体抗炎药、钙剂、免疫球蛋白及糖皮质激素等对症支持来控制病情。 2019年9月，FDA批准勃林格殷格翰的Ofev（nintedanib，尼达尼布）用于延缓系统性硬化症相关间质性肺病（SSc-ILD）成人患者的肺功能下降。该药是一种口服小分子酪氨酸激酶抑制剂，通过竞争性抑制成纤维细胞生长因子受体、血管内皮生长因子受体、血小板源性生长因子受体等受体酪氨酸激酶，阻断对成纤维细胞的增殖、迁徙和转换起关键作用的信号传导，从而抑制肺纤维化病变。 2021年3月，FDA批准罗氏IL-6受体抑制剂Actemra/RoActemra（tocilizumab，托珠单抗）皮下注射液，用于延缓SSc-ILD成人患者肺功能下降的速度。这使Actemra/RoActemra成为FDA批准的第一款用于治疗SSc-ILD的生物疗法。在研SSc药物进展据不完全统计，目前全球已出现多款在研SSc新药，详见下表。在研SSc新药作用靶点多样，且药物类型也非常多样化，涉及化药、单抗、干细胞疗法等。具体品种来看，Anifrolumab是一款首创Ⅰ型干扰素受体（IFNAR1）拮抗剂，已被批准用于治疗系统性红斑狼疮。研究表明，I型干扰素能够直接影响T细胞的增殖与活化，因此，Anifrolumab作为一种中和干扰素的药物，能够减少SSc患者T细胞的活化与增值，从而达到治疗SSc的目的。目前，Anifrolumab治疗SSc的3期临床试验正在进行中。贝利尤单抗是GSK研发的一款靶向B淋巴细胞刺激因子（BLyS）的单克隆抗体，通过特异性结合BLyS抑制B细胞的存活和增殖，其静脉注射剂已被批准成人和儿童系统性红斑狼疮，以及活动性狼疮肾炎。与静脉注射相比，贝利尤单抗的皮下注射剂型具有缩短治疗时间和提高治疗便利性的潜力。目前，贝利尤单抗皮下注射液正在国内开展一项针对SSc-ILD成人患者的国际多中心（含中国）2/3期研究。 Amlitelimab由赛诺菲与ImmuNext合作开发，是一种皮下注射的全人源化、非耗竭性单克隆抗体，通过与OX40L结合，旨在恢复促炎及调节性T细胞之间的免疫稳态，从而有潜力治疗许多免疫介导及炎症性疾病。此外，amlitelimab在抑制T细胞依赖性炎症的同时，不会导致免疫细胞的清除，从而潜在避免了免疫抑制的副作用。Amlitelimab被开发用于治疗特应性皮炎、哮喘、多发性硬化、化脓性汗腺炎、SSc等自免疾病，其中针对SSc相关间质性肺疾病（SSc-ILD）的临床试验处于2期阶段。 BI 685509是一种不依赖一氧化氮的可溶性鸟苷酸环化酶（sGC）刺激剂，可增加环磷酸鸟苷（cGMP）的产生。cGMP升高与血管舒张、血管床中的适当内皮功能以及抗纤维化、抗增殖和抗炎作用相关。BI 685509可能针对导致SSc表现的基础血管病变和纤维化。目前，BI 685509针对SSc的临床试验处于2期阶段。 FT011是一种口服药物，旨在阻断GPR68蛋白受体的活性。GPR68是一种特定的G蛋白偶联受体(GPCR)，可介导与炎症和纤维化相关的信号通路，其在健康组织中处于沉默状态，但在受伤或患病后被激活。证据表明：GPR68在导致炎症和纤维化的多个下游通路中发挥作用。临床试验数据显示：FT011在改善肺功能和缓解身体残疾方面表现出显著疗效。2024年7月，FT011被EMA授予孤儿药资格，用于SSc。 RY_SW01是一款人脐带间充质干细胞来源的干细胞疗法。与传统疗法相比，脐带间充质干细胞（MSCs）可以通过多通路进行免疫调节，并分泌细胞因子达到抗纤维化的作用；安全性方面，不会引起类似免疫抑制剂带来的不良反应。2023年8月，RY_SW01治疗SSc的临床试验申请获CDE批准。 CABA-201是Cabaletta Bio开发的一款使用4-1BB共刺激信号的全人源CD19 CAR-T疗法，有望成为B细胞驱动的自身免疫性疾病的潜在治疗方法。2024年1月，CABA-201治疗SSc的1期临床试验启动。2024年3月，该药被FDA授予治疗SSc的孤儿药资格。 VUM02是中源协和自主研发的冷冻保存型干细胞制剂，是由经筛选的健康新生儿脐带组织通过体外分离、扩增、收获、冻存后制备的人脐带源间充质干细胞（UC-MSC）候选药物。2024年9月，VUM02治疗SSc的临床试验申请获CDE批准。 RJMty19是瑞顺生物基于人源化CD19-CAR全球专利开发的一款创新现货通用型第二代DNT细胞治疗候选药物被，被开发用药治疗难治性系统性红斑狼疮、复发/难治性B细胞非霍奇金巴瘤、CD19阳性成人复发/难治性B细胞急性淋巴细胞白血病和SSc等。今年9月，RJMty19治疗SSc的临床试验申请获CDE批准。此外，Blinatumomab也被开发用于治疗SSc。该药是一种双特异性抗体结构，通过结合T细胞上的CD3和B细胞上的CD19，介导T细胞与B细胞的相互作用，导致后者被前者破坏。Blinatumomab已被证实能引起血液肿瘤患者的B细胞耗竭及免疫球蛋白水平下降。 2024年6月，来自德国慕尼黑大学附属医院(LMU)血液科的Marion Subklewe等人在《European Journal Of Cancer》杂志上发表了题为"Application of blinatumomab, a bispecific anti-CD3/CD19 T-cell engager, in treating severe systemic sclerosis: A case study"的案例研究论文结果显示：Blinatumomab安全有效，治疗过程中所有剂量下的耐受性良好，SSc患者的症状得到有效改善。总结整体来看，近些年罕见病系统性硬化症（SSc)的治疗进展有限，最新获批的两款药物--尼达尼布、托珠单抗也仅被批准用于延缓系统性硬化症相关间质性肺病（SSc-ILD）成人患者的肺功能下降，并不能从根上治愈SSc。纵观在研SSc药物，其作用靶点非常多样，这从一定程度上可以看出SSc的发病机制并不十分明确。期待在药企的不懈努力下，SSc治疗早日迎来重大突破。 END END END END 【智药研习社直播预告】来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com ▼更多制药资讯，请关注CPHI制药在线▼ 点击阅读原文，进入智药研习社~

临床研究细胞疗法免疫疗法临床申请

2024-09-16

·GlobeNewswire-Health Care

Certa Therapeutics Announces International Non-Proprietary Name for its First-in-class GPR68 Inhibitor Asengeprast (FT011)

MELBOURNE, Australia, Sept. 16, 2024 (GLOBE NEWSWIRE) -- Certa Therapeutics (Certa), a biotechnology company developing innovative precision therapies for patients with fibrotic diseases, today announces that its lead candidate FT011 has been granted the International Non-Proprietary Name (INN) of ‘asengeprast’ by the World Health Organisation (WHO). Commonly known as a generic name, an INN is a globally recognised, unique name for a pharmaceutical substance or active ingredient. Certa has pioneered drug development targeting GPR68, an important but previously undrugged membrane GPCR receptor, showing it to be a master switch of fibrosis. Asengeprast is a novel, first-in-class oral GPR68 antagonist being developed for the treatment of chronic fibrosis in multiple organs. An extensive body of data demonstrates promising efficacy in multiple in vitro and in vivo models of inflammatory and fibrotic disease. Phase I and IIa clinical studies in patients with systemic sclerosis (SSc) have already demonstrated favourable efficacy, safety and pharmacokinetics. SSc is a chronic, progressive, and potentially life-threatening autoimmune disease characterised by inflammation and fibrosis (scar tissue formation) in the skin and in various internal organs - commonly lungs, kidneys and heart. Skin fibrosis is the distinguishing feature of SSc and is associated with significantly reduced function and disability in patients. Currently, there are no treatments on the market that effectively stop or reverse scarring in the skin and organs. Professor Darren Kelly Certa Therapeutics CEO and founder said, “The granting of an INN for our lead drug candidate asengeprast is another important step in its development of this important therapy and follows the granting of EU and US Orphan Drug status and an FDA Fast Track Designation. We are continuing to drive the clinical development of asengeprast and believe it has the potential to address a critical need for people living with SSC, a debilitating condition with the highest mortality amongst rheumatic diseases.” Certa is planning for a Phase IIb confirmatory SSc clinical trial with asengeprast, bringing the company closer to providing better treatment options for patients with fibrosis. It is also developing biomarkers and gene signatures to identify patients most likely to respond to treatment to ensure the best outcomes for those with fibrosis. Certa has a portfolio of GPR68 inhibitors designed to target other organs being developed for the treatment of a number of fibrosis driven kidney diseases. For further information please contact Media – AustraliaKirrily Davis, E: kdavis@bcpvc.com M: +61 (0)401 220228 Media - InternationalSue Charles, Charles Consultants E: sue.charles@charles-consultants.com M: +44 (0)7968 726585 About Certa Therapeutics Certa Therapeutics is a clinical-stage biotechnology company focused on improving lives by treating patients with debilitating diseases via novel targeted therapies. Certa Therapeutics has designed a platform of candidate drugs and validated the role of GPR68, a defined G protein-coupled receptor (GPCR) receptor which mediates signalling pathways associated with inflammation and fibrosis. GPR68 is silent in healthy tissue but activated following injury or disease. Evidence demonstrates the role of GPR68 on multiple downstream pathways causing inflammation and fibrosis. These targeted drug candidates have established proof of concept as potential treatments for multiple fibrotic diseases including serious and chronic conditions impacting the kidney, lung, eye, skin, and heart. The morbidity and mortality impact of fibrotic diseases is substantial, ultimately causing 45% of all deaths globally. Significant breakthroughs are urgently needed in this field, addressing a market worth more than US$15B annually. The company is seeking to combine its innovative therapeutics with biomarkers and genetic analysis to identify those patients most likely to benefit from treatment, providing potential for a precision therapy. Asengeprast (FT011) is an investigational product which has not received marketing authorisation or approval by any regulatory agency, including the US Food and Drug Administration, the European Medicines Agency, or the Australian Therapeutic Goods Agency. The investigational drug products being developed by Certa Therapeutics are undergoing clinical studies to evaluate the safety and effectiveness in humans. In the company’s lead program, asengeprast is being developed as a novel, first-in-class oral therapy for the treatment of systemic sclerosis (scleroderma) and has successfully completed a multi-national, double-blinded randomised controlled trial. In addition to being granted EMA Orphan Drug Designation, asengeprast has been awarded Orphan Drug Designation and Fast Track Designation from the FDA. https://certatherapeutics.com/ Follow us on LinkedIn : https://www.linkedin.com/company/certa-therapeutics/

孤儿药快速通道临床2期临床1期

100 项与 Asengeprast 相关的药物交易

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适应症	最高研发状态	国家/地区	公司	日期
弥漫性硬皮病	临床2期	澳大利亚	Certa Therapeutics Pty Ltd.初创企业	2021-07-19
弥漫性硬皮病	临床2期	荷兰	Certa Therapeutics Pty Ltd.初创企业	2021-07-19
弥漫性硬皮病	临床2期	波兰	Certa Therapeutics Pty Ltd.初创企业	2021-07-19
弥漫性硬皮病	临床2期	西班牙	Certa Therapeutics Pty Ltd.初创企业	2021-07-19
弥漫性硬皮病	临床2期	乌克兰	Certa Therapeutics Pty Ltd.初创企业	2021-07-19
青光眼	临床1期	澳大利亚	OccuRx Pty Ltd初创企业	2019-05-13
糖尿病肾病	临床1期	澳大利亚	Fibrotech Therapeutics Pty Ltd.	2013-05-20
系统性硬皮病	临床前	美国	Certa Therapeutics Pty Ltd.初创企业	2023-10-10
慢性肾病	临床前	-	Certa Therapeutics Pty Ltd.初创企业	2022-11-03
免疫球蛋白a肾病	临床前	澳大利亚	Shire Plc	2007-04-26

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04647890 (CTgov)	临床2期	弥漫性硬皮病 \| 系统性硬皮病	30	FT011 (FT011 200mg)	願鬱鑰憲製壓壓膚顧鏇(鬱艱廠憲遞糧構餘鹹艱) = 糧鑰糧壓積鹽獵憲積構廠鏇鏇淵鬱製鏇遞蓋遞 (簾網憲壓鑰繭膚範膚構, 壓餘積鹽壓獵獵餘艱廠 ~ 鹽繭鑰製繭齋淵觸願餘) 更多	-	2023-12-20
				FT011 (FT011 400mg)	願鬱鑰憲製壓壓膚顧鏇(鬱艱廠憲遞糧構餘鹹艱) = 鬱顧觸積範鹽醖網鏇觸廠鏇鏇淵鬱製鏇遞蓋遞 (簾網憲壓鑰繭膚範膚構, 構築網遞餘餘範廠糧衊 ~ 簾製蓋廠糧遞選簾衊糧) 更多