MOSAIC - A Phase 2b, Randomized, Double-Blind, Placebo-Controlled, Parallel Group, Multicenter Study Evaluating the Efficacy and Safety of Selonsertib in Subjects With Moderate to Advanced Diabetic Kidney Disease

The primary objective of this study is to evaluate whether selonsertib (SEL) can slow the decline in kidney function in participants with moderate to advanced diabetic kidney disease (DKD).

Start Date24 Jul 2019

Sponsor / Collaborator

Gilead Sciences, Inc.

ACTRN12618001377224 / RecruitingPhase 1

A Phase 1b, Randomized, Blinded, Placebo-Controlled Study toEvaluate the Effect of Selonsertib on Renal Function as Assessedby Markers of Glomerular Filtration Rate in Subjects with ChronicKidney Disease

Start Date31 Jul 2018

Sponsor / Collaborator

Gilead Sciences, Inc.

NCT03449446 / CompletedPhase 2

A Phase 2, Randomized, Double-Blind, Placebo-Controlled Study Evaluating the Safety and Efficacy of Selonsertib, GS-0976, GS-9674, and Combinations in Subjects With Bridging (F3) Fibrosis or Compensated Cirrhosis (F4) Due to Nonalcoholic Steatohepatitis (NASH)

The primary objectives of this study are:
To assess the safety and tolerability of selonsertib (SEL), firsocostat (FIR) and cilofexor (CILO), administered alone or in combination, in participants with bridging fibrosis or compensated cirrhosis due to NASH
To evaluate changes in liver fibrosis, without worsening of NASH

Start Date21 Mar 2018

Sponsor / Collaborator

Gilead Sciences, Inc.

100 Clinical Results associated with Selonsertib

100 Translational Medicine associated with Selonsertib

100 Patents (Medical) associated with Selonsertib

Literatures (Medical) associated with Selonsertib

31 Dec 2024·JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY

Synthesis and biological evaluation of quinoxaline derivatives as ASK1 inhibitors

Article

Author: Wang, Zengtao ; Chen, Zhongwen ; Lan, Pingping ; Wang, Tiantian ; Han, Xiaorui ; Liu, Hua ; Chen, Qianfeng

Inhibiting apoptosis signal regulated kinase 1 (ASK1) is an attractive strategy for treating diseases such as non-alcoholic steatohepatitis and multiple sclerosis. Here, we report the discovery of a dibromo substituted quinoxaline fragment containing 26e as an effective small-molecule inhibitor of ASK1, with an IC₅₀ value of 30.17 nM. In addition, the cell survival rate of 26e at different concentrations was greater than 80%, especially at 0.4 μM. Its cell survival rate was significantly higher than GS-4997, indicating its good safety in normal human liver LO2 cells. The Oil Red O staining experiment showed that 26e decreased the lipid droplets in a dose-dependent manner. Further biochemical analyses revealed that 26e could reduce the content of T-CHO, LDL, and TG in FFA-induced LO2 cells, and had the potential to treat non-alcoholic fatty disease. These findings provide a good choice for the future development of ASK1 inhibitors.

14 Dec 2024·CARDIOVASCULAR RESEARCH

Cardiac tumour necrosis factor receptor-associated factor 7 mediates the ubiquitination of apoptosis signal-regulating kinase 1 and aggravates cardiac hypertrophy

Article

Author: Qiu, Hong-Liang ; Tang, Qi-Zhu ; Xia, Hong-Xia ; Wang, Sha-Sha ; Wang, Zhao-Peng ; Che, Yan ; Zhou, Heng ; Feng, Yi-Zhou ; Yuan, Yuan ; Hu, Man-Li ; Liu, Yu-Ting

Abstract:

Aims:

Cardiac remodelling is a common pathophysiological process in the development of various cardiovascular diseases, but there is still a lack of effective interventions. Tumour necrosis receptor-associated factor 7 (TRAF7) belongs to the tumour necrosis factor receptor-associated factor family and plays an important role in biological processes. Previous studies have shown that TRAF7 mutations lead to congenital defects and malformations of the heart. However, the molecular mechanisms of TRAF7 in the underlying pathogenesis of pathological cardiac hypertrophy remain unknown. We aim to study the molecular mechanisms and effects of TRAF7 in cardiac remodelling and whether it has the potential to become a therapeutic target for cardiac remodelling.

Methods and results:

The pressure overload–induced cardiac hypertrophy model in mice was established via transverse aortic constriction (TAC) surgery, and cardiomyocytes were treated with phenylephrine (PE) to induce hypertrophic phenotype. Levels of cardiac dysfunction and remodelling were measured with echocardiography and tissue or cell staining. RNA sequencing, western blot, qRT–PCR, co-immunoprecipitation, and in vivo ubiquitination assays were used to explore the molecular mechanisms. The results showed that the expression of TRAF7 increased gradually during the development of hypertrophy. Accordingly, TRAF7 significantly exacerbated the PE-induced enlargement of primary neonatal Sprague-Dawley rat cardiomyocytes, whereas TRAF7 knockdown alleviated the hypertrophic phenotype in primary cardiomyocytes. Cardiac-specific overexpression of TRAF7 accelerated hypertrophic phenotype in mice and cardiac-specific Traf7 conditional knockout mice improved hypertrophic phenotype induced by TAC. Mechanistically, TRAF7 directly interacted with apoptosis signal-regulating kinase-1 (ASK1) and promoted ASK1 phosphorylation by mediating the K63-linked ubiquitination of ASK1 in response to PE stimulation, which then promoted ASK1 activation and downstream signalling during cardiac hypertrophy. Notably, the pro-hypertrophic effect of TRAF7 was largely blocked by GS4997 in vitro and cardiac-specific Ask1 conditional knockout in vivo.

Conclusion:

In summary, we identified TRAF7 as an essential regulator during cardiac hypertrophy, and modulation of the regulatory axis between TRAF7 and ASK1 could be a novel therapeutic strategy to prevent this pathological process.

01 Dec 2024·JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY

Selonsertib in Patients with Diabetic Kidney Disease

Article

Author: Chen, Fang ; Kustra, Robert ; Kuo, Albert ; Heerspink, Hiddo J.L. ; Chertow, Glenn M. ; Perkovic, Vlado ; Pergola, Pablo E. ; Kashihara, Naoki ; Petrovic, Vladimir ; Ishida, Julie H. ; Rossing, Peter ; Mahaffey, Kenneth W. ; Patel, Uptal D. ; Tuttle, Katherine R.

Key Points:

In a randomized, placebo-controlled, phase 2b study, we compared the effects of selonsertib with placebo on eGFR decline in people with type 2 diabetes and CKD.Patients taking selonsertib had slower eGFR decline but were more likely to reach a composite kidney outcome and report AKI.A larger trial with longer-term follow-up would more precisely assess the relative benefits and risks of selonsertib in this setting.

Background:

Selonsertib is an apoptosis signal–regulating kinase 1 inhibitor that reduces inflammation, fibrosis, and apoptosis. The MOSAIC study evaluated whether selonsertib attenuated kidney function decline in patients with diabetic kidney disease.

Methods:

We conducted a phase 2b study in adults with type 2 diabetes and eGFR 20 to <60 ml/min per 1.73 m2 with urine albumin-creatinine ratio 150–5000 mg/g on maximum tolerated dose of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. To account for an acute selonsertib-related decrease in serum creatinine–based eGFR (eGFRcr), patients entered a 4-week selonsertib run-in period to establish treatment-specific baseline eGFRcr. Patients were randomized 1:1 to selonsertib 18 mg or matching placebo once daily. We followed all participants up until the last randomized participant completed 48 weeks of follow-up. The primary efficacy outcome was the difference in eGFRcr slopes from treatment-specific baselines to week 84, evaluated at a prespecified two-sided P = 0.30. We also evaluated kidney clinical events (eGFRcr ≥40% decline from pre–run-in baseline, kidney failure, or death due to kidney disease) and adverse events.

Results:

In total, 310 patients were randomized (selonsertib n=154, placebo n=156; 68% male, mean age 65 years, mean baseline eGFRcr 35 ml/min per 1.73 m2). Mean difference between selonsertib and placebo eGFRcr slopes at week 84 was 1.20 ml/min per 1.73 m2 per year (95% confidence interval, −0.41 to 2.81; P = 0.14). Kidney clinical events occurred in 17% (26/154) of patients randomized to selonsertib and 12% (19/156) of those randomized to placebo (difference 4.7%; 95% confidence interval, −6.3% to 15.9%). The most common investigator-reported adverse event was AKI (selonsertib 11.0/100 and placebo 5.9/100 patient-years).

Conclusions:

Selonsertib attenuated the decline in eGFRcr over up to 84 weeks; however, it resulted in a numerically higher number of patients reaching a kidney clinical event and a numerically higher rate of investigator-reported AKI.

Clinical Trial registry name and registration number::

Study to Evaluate the Efficacy and Safety of Selonsertib in Participants With Moderate to Advanced Diabetic Kidney Disease (MOSAIC), NCT04026165.

News (Medical) associated with Selonsertib

01 Jun 2023

·www.fiercebiotech.com

Genfit adds 3rd liver failure asset to roster in $107M biobucks deal with Seal Rock

Genfit now has three candidates aimed at acute-on-chronic liver failure. Genfit has added a third liver failure candidate to its portfolio courtesy of a licensing deal with Seal Rock Therapeutics potentially worth up to 100 million euros ($107 million) in biobucks. The asset in question is an injectable form of Seal Rock’s ASK1 inhibitor SRT-015, for which Genfit has secured the rights in liver disease. France-based Genfit has its sights set on entering the clinic with the candidate in the second half of next year, with a proof-of-concept study in acute-on-chronic liver failure (ACLF) penciled in for 2025. Apoptosis signal-regulating kinase 1 (ASK1) is a member of the MAP kinase family. Inhibiting ASK1 has been shown to block lipopolysaccharide-associated hyperinflammatory response as well as reduce the release of proinflammatory cytokines, reduce fibrosis and protect macrophage mitochondrial function, Genfit explained in the postmarket release yesterday. Animal models and clinical trials have already shown benefits of this mechanism across a wide range of organ diseases, including of the kidney, liver, brain and cardiopulmonary system, the biotech added. These drugs haven’t always lived up to the hype, however. Gilead’s ASK1 inhibitor selonsertib flunked a couple of phase 3 trials in nonalcoholic steatohepatitis, the same condition for which Seal Rock had been developing SRT-015. Eyeing an ACLF market estimated to total $4 billion in the U.S. and five major European countries alone, the Seal Rock deal means Genfit now has three candidates targeting this space. Those include VS-01, which is in a phase 2 trial for adults with ACLF grades 1 and 2 and ascites, as well as NTZ, which has completed a pair of phase 1 studies in renal and hepatic impairment. Genfit is now readying NTZ for a phase 2 in ACLF. Genfit CEO Pascal Prigent said today’s licensing agreement “marks an additional milestone in the execution of our development strategy in liver diseases with high unmet medical needs.” “ACLF is a complex disorder that will likely require the combination of different approaches and with this acquisition, we continue to strengthen our leadership in this indication,” Prigent added. “Considering its liver-centric activity, the potential for multi-organ benefits and the breadth of evidence supporting further development in ACLF, we strongly believe in the potential of SRT-015.” While no upfront payment was mentioned in the release, Seattle-based Seal Rock is in line for up for 100 million euros in regulatory, clinical and commercial milestone payments alongside tiered royalties. Genfit’s remaining therapeutic pipeline includes the dual PPAR agonist elafibranor, which is undergoing late-stage studies for primary biliary cholangitis and has been licensed by Ipsen. There's also GNS561, a PPT1 inhibitor that has previously completed a phase 1 trial and is now being developed for bile duct cancer, and VS-02, a preclinical urease inhibitor the biotech hopes to progress for hepatic encephalopathy.

Phase 1License out/inPhase 2

31 May 2023

·www.prnewswire.com

Seal Rock Therapeutics Announces Out-Licensing Agreement with GENFIT for Development of Injectable Formulation of SRT-015 for Acute-on-Chronic Liver Disease (ACLF)

Seal Rock eligible to receive payments up to €100 million, including regulatory, clinical, and commercial milestone payments, plus tiered royalties SEATTLE, May 31, 2023 /PRNewswire/ -- Seal Rock Therapeutics, Inc., a clinical stage company developing first-in-class and best-in-class kinase inhibitors, today announced it has entered into an out-licensing agreement with GENFIT (Nasdaq and Euronext: GNFT) for the development of an injectable formulation of SRT-015 for acute liver disease, including Acute-on-Chronic Liver Failure (ACLF). Under the agreement, Seal Rock Therapeutics is eligible for payments up to €100 million, including regulatory, clinical, and commercial milestone payments, plus tiered royalties. SRT-015, a highly optimized, second generation, liver-selective inhibitor of Apoptosis Signal-reducing Kinase 1 (ASK1). It is being developed by Seal Rock Therapeutics, in an oral formulation, as a treatment for severe acute alcoholic hepatitis as well as orphan liver diseases and NASH. "We're excited to announce this licensing deal with GENFIT that will accelerate the development of an injectable formulation of our second-generation ASK1 inhibitor SRT-015 for ACLF, a liver disease with high unmet need," said Neil McDonnell, CEO of Seal Rock Therapeutics. "At Seal Rock, we remain focused on initiating a Phase 2a trial of oral SRT-015 for severe alcoholic hepatitis. We will also continue development of our first-in-class LRRK2/ASK1 dual kinase inhibitors for Parkinson's Disease and ALS." "Considering its liver-centric activity, the potential for multi-organ benefits and the breadth of evidence supporting further development in ACLF, we strongly believe in the potential of SRT-015," said Pascal Prigent, CEO of GENFIT. "We are pleased to have this opportunity to develop a new, injectable formulation of SRT-015 for Acute-on-Chronic Liver Failure (ACLF)." About SRT-015 SRT-015 is a second-generation inhibitor of ASK1 developed internally by Seal Rock Therapeutics. Optimized to overcome the liabilities of first-generation ASK1 inhibitors such as selonsertib, and with a liver-preferential distribution, SRT-015 is positioned as a first-in-class product candidate for NASH and AH. About Seal Rock Therapeutics Seal Rock Therapeutics is a privately held, clinical stage company based in Seattle focused on developing first-in-class and best-in-class treatments for severe diseases with limited or no available therapies. Seal Rock is led by an experienced management team with a track record of successful drug discovery, development and commercialization. The company's clinical-stage lead product candidate, SRT-015, is a highly optimized, first-in-class ASK1 inhibitor. Seal Rock is also developing preclinical-stage brain-penetrant ASK1/LRRK2 dual kinase inhibitors for treatment of neurodegenerative conditions such as Parkinson's disease and ALS. For more information, please visit Media Contact: Julie Rathbun Rathbun Communications [email protected] 206-769-9219 SOURCE Seal Rock Therapeutics

License out/inPhase 2

02 May 2023

·www.prnewswire.com

Viscient Biosciences Announces First Drug Discovered in 3D Bioprinted Models

Company's NASH Drug Expected to Enter Clinic in 2024 SAN DIEGO, May 2, 2023 /PRNewswire/ -- Viscient Bio, Inc. ("Viscient") today announced it has identified the world's first drug candidate discovered primarily using 3D bioprinted tissue models of disease formed from human cells. Viscient expects to develop the drug to treat non-alcoholic steatohepatitis (NASH), a growing epidemic disease that is believed to affect more than 10% of the US population. NASH can often lead to hepatocellular carcinoma or liver failure. Due to the devastating effects of NASH on patients and its wide prevalence, analysis have projected future pharma industry revenues for the drug in the tens of billions of dollars per year. Continue Reading Viscient's lead compound is an orally delivered small molecule designed to hit a novel target identified in 3D bioprinted and other 3D tissue models of disease. In preclinical studies, the drug has proven to be well tolerated. In Viscient's models of disease, the compound shows reduction of fibrosis as measured by histological evidence similar to that used for human liver biopsy. Using the same model, fibrosis reduction is also seen for obeticholic acid and resmetirom, while no fibrosis reduction is seen for drugs such as cenicriviroc, selonsertib, and elafibranor. The newly discovered target is predominantly expressed in liver tissue. Failed NASH drugs never would have been put in humans based on what can be clearly seen in these models. Tweet this "It is long past time to displace the model of drug development reliant on proof of activity in animals," said Viscient chief executive officer Keith Murphy. "Viscient's trailblazing work has resulted in 3d cellular human models of disease in which the performance of previously tested compounds has matched clinical results. Failed NASH drugs never would have been put in humans based on what can be clearly seen in these models. Our novel compound shows fibrosis reduction in these models, as do NASH drugs known to work in Phase 3, and we are excited to move this lead program forward." The lead compound's clear reduction of fibrosis in Viscient's NASH models is promising because Viscient's 3D models of NASH have shown extremely high correlation with clinical results in patients. The model demonstrates fibrosis reduction for known clinical compounds tested by pharma companies that have that effect in humans, while revealing lack of fibrosis reduction for compounds that failed in Phase 2 or Phase 3 for NASH. The model is accurate in predicting both successes and failures among clinical compounds tested to date. The gene expression of Viscient's models is also well correlated with that seen in disease samples from patients. Though tested post-hoc, the results are not backfit, as the model was finalized before testing of any clinical compounds was conducted. According to the Biotechnology Innovation Organization's 2021 report, only 7.9% of drugs that enter clinical trials are approved for human use. Viscient Biosciences believes that we can achieve a significantly better clinical translation rate than that using more relevant 3D human tissue models of disease, leading to more successes and lower drug development costs per approved drug. Viscient is leading the world in creation of human tissue models with accurate disease relevance, and demonstrating the application of these models to drug development at every stage. About Viscient Biosciences Viscient Biosciences is an early-stage biotechnology company that is developing novel therapies for NASH and other liver diseases. Its lead compound, built to a novel target discovered in proprietary 3D models of human liver disease, is expected to enter the clinic in 2024. Viscient's 3D models of NASH have shown extremely high correlation with clinical results in patients, demonstrating fibrosis reduction for compounds that have that effect in humans while revealing lack of fibrosis reduction for compounds that failed in Phase 2 or Phase 3 for NASH. The gene expression of Viscient's models is also well correlated with that seen in disease samples from patients. Utilizing these 3D human tissues as dynamic models of healthy and diseased human biology for drug development, the company identifies opportunities both for novel therapeutic development and the in-licensing and repurposing of drugs. SOURCE Viscient Bio, Inc.

Clinical Result

100 Deals associated with Selonsertib

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KEGG	Wiki	ATC	Drug Bank
D10988	-	-	DB14916

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Compensated cirrhosis	Phase 3	US	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	JP	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	AU	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	AT	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	BE	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	CA	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	FR	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	DE	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	HK	Gilead Sciences, Inc.	30 Jan 2017
Compensated cirrhosis	Phase 3	IN	Gilead Sciences, Inc.	30 Jan 2017

Clinical Result

Indication

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Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04026165 (MOSAIC, Pubmed \| J Am Soc Nephrol)	Phase 2	Diabetic Nephropathies eGFR \| urine albumin-creatinine ratio	310	Selonsertib 18 mg	etawctsiae(emgzkqstmt) = zxfzugqggh fxfyqyxctw (tmdkvenmtp, -0.41 to 2.81) View more	Positive	01 Dec 2024
				Placebo	fvkbhctynn(bfahtexjli) = iyngvqyjuk knxqinitsr (ufgfvpdnmp ) View more
NCT04026165 (MOSAIC, CTgov)	Phase 2	Diabetic Nephropathies	384	SEL (Randomized SEL 18 mg)	fdnuzxazlx(cjuccjnxtc) = zfkojfwoas qorganknfl (zlzygkwdbf, lpweptkpnu - jzwsguwyzh) View more	-	21 Dec 2022
				placebo+SEL (Randomized Placebo)	fdnuzxazlx(cjuccjnxtc) = tzwvcvaqvs qorganknfl (zlzygkwdbf, guyivaudzg - ikpxphrxnt) View more
MOSAIC (ASN2022)	Phase 2	Diabetic Nephropathies type 2 diabetes mellitus \| eGFR \| UACR ... View more	310	Selonsertib 18 mg	bwgvmuryxh(jmszbmjrog) = nuxrazuvds mahbgbohvg (yxkazwhspe, -0.41 to 2.81) View more	Positive	04 Nov 2022
				Placebo	buypkkmqva(qysakgptjm) = axvyopnjko bnienrywod (dbvgtjdgat ) View more
NCT03053050 \| NCT03053063 (STELLAR, Pubmed \| Clin Gastroenterol Hepatol) Manual	Phase 3	Fibrosis	3,207	Selonsertib (whites)	prruqphjib(kqplklnlws) = scgchzibes rmsxpkilux (ewdoqanybc ) View more	Positive	21 Jan 2022
				Selonsertib (Asians)	prruqphjib(kqplklnlws) = ojosalxtrw rmsxpkilux (ewdoqanybc ) View more
NCT02509624 (CTgov)	Phase 1	Diabetic Nephropathies	52	selonsertib (Cohort 1: Moderate Hepatic Impairment)	yfmtxjbmmh(gbyhowptjr) = eqzjxiicyq tgbdrjklvc (usdgdrllus, opiaxpgumv - mbmmvcnzwo) View more	-	27 Jan 2021
				selonsertib (Cohort 2: Severe Hepatic Impairment)	yfmtxjbmmh(gbyhowptjr) = ivzfadzucb tgbdrjklvc (usdgdrllus, bomxrpbrhc - imtlhwrdnt) View more
NCT03449446 (ATLAS, CTgov)	Phase 2	Nonalcoholic Steatohepatitis \| Fibrosis \| Compensated cirrhosis	395	Placebo to match SEL	pfovwhpzdy(hlkbhxrptl) = eromxjkscv nucemocapr (mjyccjcqhx, iyqcxiryes - andowtjhww) View more	-	03 Dec 2020
ASN2020	Phase 2	Fanconi Syndrome sTNFR1 \| TNF α \| IP-10 ... View more	-	Selonsertib (SEL)	zgaxrsyqeb(jpmspfeuyb) = efqejmpduq gijjmlbgje (ivqywdueuf ) View more	Positive	19 Oct 2020
				Selonsertib (Control (no treatment))	zgaxrsyqeb(jpmspfeuyb) = dcjnbxqzex gijjmlbgje (ivqywdueuf ) View more
NCT03053063 (STELLAR-4, EASL2020)	Phase 3	Nonalcoholic Steatohepatitis	644	Selonsertib	fwucsioisp(ydbafozjda) = kdbigfudcg zogixcjxsd (jsldojpitk )	-	27 Aug 2020
				Placebo	dktiwsmbgw(ywjubhfwre) = csemngavac zudsuzfzwt (cavahlxzyp )
NCT03053050 \| NCT03053063 (STELLAR, Pubmed \| J Hepatol)	Phase 3	Nonalcoholic Steatohepatitis \| Fibrosis	-	Selonsertib 18 mg	hexnijtcbv(zenqedexls) = tllcjkiejx torhlkzraa (dhakgdyocb )	Negative	01 Jul 2020
				Selonsertib 6 mg	hexnijtcbv(zenqedexls) = wksvwkxaov torhlkzraa (dhakgdyocb )
NCT03053050 (STELLAR-3, CTgov)	Phase 3	Nonalcoholic Steatohepatitis	808	Placebo to match SEL 6 mg+SEL (SEL 18 mg)	mthgwpmibk(nlqikjebhh) = xrlkfuwlzx jflddddsxy (foggjhdbkj, uuaypybghc - nzumbsrqhu) View more	-	29 Jun 2020
				Placebo to match SEL 18 mg+SEL (SEL 6 mg)	mthgwpmibk(nlqikjebhh) = yavrdhhtrc jflddddsxy (foggjhdbkj, ubgbdmkcfd - fufgvsqwre) View more

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