Latest news with #Rein
Scoop
25-05-2025
- Business
- Scoop
Budget 2025: Sole Trader Feels ‘Ripped Off' By Government's KiwiSaver Cuts
Article – RNZ The budget move to halve the government's KiwiSaver contributions has been described as a blow to sole traders. Anan Zaki, Business reporter The budget move to halve the government's KiwiSaver contributions has been described as a blow to sole traders. The government contribution would be cut from $521 to just over $260 – provided there was a minimum of $1042 saved over a year, and those earning more than $180,000 would now miss out altogether. The government said this is to make sure the scheme's costs to the taxpayer 'remain sustainable'. Wellington-based personal trainer Carl Rein believed it would affect him long-term. 'I'm in my 30s, so I've got at least 30-plus years to go before I'm even going to be able to access it,' Rein said. 'So all of that accumulated interest that I would benefit from later on, and it would give me greater security later on in life, is now not going to be there.' Rein said the move made it 'disheartening' to be involved in KiwiSaver, and he felt 'ripped off'. He was also concerned it opened the door for government contributions to become zero. Rein's comments came alongside criticism of the policy from sole trader tax platform Hnry. Hnry chief executive James Fuller said the government's decision posed risks to the country's 400,000 sole traders. 'The danger is that sole traders switch off from KiwiSaver entirely and then potentially look at more risky ways to try and prop up the income they would have got from their retirement savings that the government was contributing to,' Fuller said. 'So, it leaves a lot of questions for sole traders as to where they put their money now that they know that the government isn't backing them to contribute to KiwiSaver,' he said. Fuller said KiwiSaver was the wrong place to be looking for savings.
Scoop
25-05-2025
- Business
- Scoop
Budget 2025: Sole Trader Feels 'Ripped Off' By Government's KiwiSaver Cuts
The budget move to halve the government's KiwiSaver contributions has been described as a blow to sole traders. The government contribution would be cut from $521 to just over $260 - provided there was a minimum of $1042 saved over a year, and those earning more than $180,000 would now miss out altogether. The government said this is to make sure the scheme's costs to the taxpayer "remain sustainable". Wellington-based personal trainer Carl Rein believed it would affect him long-term. "I'm in my 30s, so I've got at least 30-plus years to go before I'm even going to be able to access it," Rein said. "So all of that accumulated interest that I would benefit from later on, and it would give me greater security later on in life, is now not going to be there." Rein said the move made it "disheartening" to be involved in KiwiSaver, and he felt "ripped off". He was also concerned it opened the door for government contributions to become zero. Rein's comments came alongside criticism of the policy from sole trader tax platform Hnry. Hnry chief executive James Fuller said the government's decision posed risks to the country's 400,000 sole traders. "The danger is that sole traders switch off from KiwiSaver entirely and then potentially look at more risky ways to try and prop up the income they would have got from their retirement savings that the government was contributing to," Fuller said. "So, it leaves a lot of questions for sole traders as to where they put their money now that they know that the government isn't backing them to contribute to KiwiSaver," he said. Fuller said KiwiSaver was the wrong place to be looking for savings.
Malaysian Reserve
19-05-2025
- Business
- Malaysian Reserve
Rein Therapeutics Presents Two Posters at the American Thoracic Society 2025 International Conference
Presentations further support the dual mechanism of LTI-03 and the development of Cav1-related peptides for the treatment of idiopathic pulmonary fibrosis (IPF) Company recently initiated RENEW Phase 2 trial evaluating the safety, tolerability and efficacy of LTI-03 in IPF AUSTIN, Texas, May 19, 2025 /PRNewswire/ — Rein Therapeutics ('Rein') (NASDAQ: RNTX), a biopharmaceutical company advancing a novel pipeline of first-in-class medicines to address significant unmet medical needs in orphan pulmonary and fibrosis indications, today announced that the Company and its collaborators presented two posters supporting the potential therapeutic effectiveness of LTI-03 in idiopathic pulmonary fibrosis (IPF) at the American Thoracic Society (ATS) 2025 International Conference. 'The presentations delivered at ATS today provide further support for the dual mechanism of our lead asset, LTI-03, which has demonstrated sustained alveolar epithelial cell survival as well as inhibition of profibrotic signaling,' said Cory Hogaboam, Ph.D., Chief Scientific Officer of Rein Therapeutics and Professor of Medicine in the Women's Guild Lung Institute at Cedars Sinai Medical Center. 'Our first presentation highlighted LTI-03's potent modulatory effects on profibrotic proteins and transcripts as well as its ability to dose-dependently increase the production of soluble receptor of advanced glycation end-products, or solRAGE, without inducing cellular necrosis. Our second presentation used alveolar organoid systems derived from donor or IPF lung epithelial cells to demonstrate LTI-03's potential to promote and sustain type 2 alveolar epithelial cell, or AEC2, viability in the IPF lung as well as its ability to support AEC2 to type 1 alveolar epithelial cell, or AEC1, differentiation. We continue to be encouraged by the body of evidence supporting the potential of LTI-03 to treat IPF, for which novel treatment options are needed. These findings are in line with the promising data that we reported from the Phase 1b trial of LTI-03 in IPF, and we look forward to sharing topline interim data from our recently initiated Phase 2 RENEW IPF trial in the first half of next year.' The first poster, entitled, 'Pre-clinical Proof-of-concept of Anti-fibrotic Activity of Caveolin-1 Scaffolding Domain Peptide LTI-03 in Ex Vivo Precision Cut Lung Slices (PCLS) from Patients with Idiopathic Pulmonary Fibrosis,' evaluates the antifibrotic effects of LTI-03, Rein's novel, multi-pathway, Caveolin-1 (Cav1)-related peptide currently in a Phase 2 trial for the treatment of IPF, and of nintedanib, a current standard of care treatment for IPF, in PCLS from 12 patients with end-stage disease. The PCLS samples were treated every 12 hours with one of 0.5 μM, 3.0 μM or 10.0 μM of LTI-03; 0.1 μM or 10.0 μM of nintedanib; or 10.0 μM of placebo, for five to seven days. Key Takeaways LTI-03 broadly attenuated profibrotic transcripts and proteins and the corresponding pathways of these factors, further supporting LTI-03's ability to inhibit profibrotic signaling. LTI-03 dose-dependently stimulated production of solRAGE, a factor indicative of AEC1 health that is a critically important aspect of IPF and has gone largely unaddressed by current treatment options. LTI-03 reduced the expression of profibrotic proteins in IPF PCLS, including Col-1α1 and platelet-derived growth factor receptor beta (PDGFRB). Unlike nintedanib, LTI-03 did not induce cellular necrosis or apoptosis. The second poster, entitled, 'Evaluating Alveolar Regenerative Properties of Caveolin Scaffolding Peptides (CSD) in Three Dimensional (3D) Alveolospheres from IPF and Normal Donor Lung Samples,' further explores the effects of LTI-03 and nintedanib on AEC2s in the normal and IPF lung. In these studies, the effects of LTI-2355, Rein's second generation Cav1-related peptide that is in preclinical development, were also examined. Eight (8) IPF lung explants and 10 normal donor lungs were processed to obtain lung epithelial cell preparations, from which AEC2s were isolated for lung organoid generation. Previous studies completed by Rein and others indicate that there is a significant decrease in the abundance of AEC2s in the IPF lung as compared to a normal lung, in turn impairing AEC2 to AEC1 differentiation and alveolar regeneration. The AEC2s from IPF and normal lung organoids were treated with 0.5 μM, 3.0 μM or 10.0 μM of either LTI-03, LTI-2355 or placebo, or 80.0 nM of nintedanib. Treatments were refreshed every other day in these lung organoid cultures for up to 28 days. Key Takeaways Cav1 scaffolding domain peptides LTI-03 or LTI-2355 sustained AEC2s in IPF lung organoids or alveolospheres, further supporting LTI-03's ability to promote alveolar epithelial cell survival. At the 10.0 μM dose, both LTI-03 and LTI-2355 increased the size of IPF alveolospheres compared to placebo at Day 28. Both LTI-03 and LTI-2355 appeared to protect normal lung alveolopheres, while nintedanib demonstrated significant growth-inhibiting or toxic effects on normal donor lung organoids at Day 28. About IPF IPF is a chronic lung disease characterized by progressive tissue scarring that prevents proper lung function. It is a progressive, fatal, age-associated lung disease affecting approximately 100,000 people in the United States1. IPF typically presents in adults 65 or older and is usually fatal within two to five years after diagnosis2. About LTI-03 and Caveolin-1 (Cav1) LTI-03 is a seven amino acid peptide, the sequence of which is derived from the caveolin scaffolding domain (CSD), an important binding region of the Cav1 protein. Cav1 normally serves a critical function in the prevention of fibrosis by maintaining a balance between pathways that both initiate and arrest lung repair and cell movement. Through the CSD, caveolin interacts with multiple signaling molecules, all of which possess a caveolin binding domain region. Cav1 expression is decreased in IPF lung tissues and has been demonstrated to decrease during the fibrotic phase of bleomycin, or BLM, lung injury in mice. Restoring the balance of important biological signals in the lung may not only slow lung function decline but could also restore healthy lung function through the protection of healthy epithelial cells. About Rein Therapeutics Rein Therapeutics is a clinical-stage biopharmaceutical company advancing a novel pipeline of first-in-class therapies to address significant unmet medical needs in orphan pulmonary and fibrosis indications. Rein's lead product candidate, LTI-03, is a novel, synthetic peptide with a dual mechanism targeting alveolar epithelial cell survival as well as inhibition of profibrotic signaling. LTI-03 has received Orphan Drug Designation in the U.S. A Phase 2 clinical trial of LTI-03 for the treatment of idiopathic pulmonary fibrosis was initiated in May 2025. Rein's second product candidate, LTI-01, is a proenzyme that has completed Phase 1b and Phase 2a clinical trials for the treatment of loculated pleural effusions. LTI-01 has received Orphan Drug Designation in the U.S. and E.U. and Fast Track Designation in the U.S. For more information, please visit the company's website at or follow them on LinkedIn and X. References1Pergolizzi, Jr., J., LeQuang, J., Varrassi, M., Breve, F., Magnusson, P., Varrassi, G., (2023). What Do We Need to Know About Rising Rates of Idiopathic Pulmonary Fibrosis? A Narrative Review and Update. Springer Nature, Published online 2023 Jan 24. Doi: 10.1007/s12325-022-02395-9.2Nathan et al. 'Long-term Course and Prognosis of Idiopathic Pulmonary Fibrosis in the New Millennium'. Chest Journal Volume 140, ISSUE 1, P221-229, July 2011. Forward-Looking Statements This press release may contain forward-looking statements of Rein Therapeutics, Inc. ('Rein', the 'Company', 'we', 'our' or 'us') within the meaning of the Private Securities Litigation Reform Act of 1995, including statements with respect to: the RENEW Phase 2 clinical trial of LTI-03, including with respect to the timing of the trial and the assumption that the Company will raise the funds necessary to conduct the trial; the therapeutic potential of LTI-03 and LTI-2355; and future expectations, plans and prospects for the Company. We use words such as 'anticipate,' 'believe,' 'estimate,' 'expect,' 'hope,' 'intend,' 'may,' 'plan,' 'predict,' 'project,' 'target,' 'potential,' 'would,' 'can,' 'could,' 'should,' 'continue,' and other words and terms of similar meaning to help identify forward-looking statements, although not all forward-looking statements contain these identifying words. Actual results may differ materially from those indicated by such forward-looking statements as a result of various important factors, including risks and uncertainties related to: the ability of the Company to obtain the cash resources to fund the RENEW Phase 2 trial through its completion and the Company's operations for the anticipated periods and the Company's ability to manage unplanned cash requirements; changes in applicable laws or regulations; the possibility that the Company may be adversely affected by other economic, business, and/or competitive factors, including risks inherent in pharmaceutical research and development, such as adverse results in the Company's drug discovery, preclinical and clinical development activities; the risk that the results of preclinical studies and early clinical trials may not be replicated in later clinical trials, including in the RENEW Phase 2 trial, or that partial results of a trial will be indicative of the full results of the trial; the Company's ability to enroll patients in its clinical trials; and the risk that any of its clinical trials may not commence, continue or be completed on time, or at all; the Company's ability to successfully integrate Qureight Ltd.'s deep-learning platform into the RENEW Phase 2 trial; decisions made by the U.S. Food and Drug Administration and other regulatory authorities, investigational review boards at clinical trial sites and publication review bodies with respect to our development candidates; as well as the risks and uncertainties discussed in the 'Risk Factors' section of the Company's Annual Report on Form 10-K for the year ended December 31, 2024, which is on file with the United States Securities and Exchange Commission (the 'SEC') and in subsequent filings that the Company files with the SEC. These forward-looking statements should not be relied upon as representing the Company's view as of any date after the date of this press release, and we expressly disclaim any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. Rein Investor Relations & Media Contact:Argot Partnersrein@
Yahoo
19-05-2025
- Business
- Yahoo
Rein Therapeutics Presents Two Posters at the American Thoracic Society 2025 International Conference
Presentations further support the dual mechanism of LTI-03 and the development of Cav1-related peptides for the treatment of idiopathic pulmonary fibrosis (IPF) Company recently initiated RENEW Phase 2 trial evaluating the safety, tolerability and efficacy of LTI-03 in IPF AUSTIN, Texas, May 19, 2025 /PRNewswire/ -- Rein Therapeutics ("Rein") (NASDAQ: RNTX), a biopharmaceutical company advancing a novel pipeline of first-in-class medicines to address significant unmet medical needs in orphan pulmonary and fibrosis indications, today announced that the Company and its collaborators presented two posters supporting the potential therapeutic effectiveness of LTI-03 in idiopathic pulmonary fibrosis (IPF) at the American Thoracic Society (ATS) 2025 International Conference. "The presentations delivered at ATS today provide further support for the dual mechanism of our lead asset, LTI-03, which has demonstrated sustained alveolar epithelial cell survival as well as inhibition of profibrotic signaling," said Cory Hogaboam, Ph.D., Chief Scientific Officer of Rein Therapeutics and Professor of Medicine in the Women's Guild Lung Institute at Cedars Sinai Medical Center. "Our first presentation highlighted LTI-03's potent modulatory effects on profibrotic proteins and transcripts as well as its ability to dose-dependently increase the production of soluble receptor of advanced glycation end-products, or solRAGE, without inducing cellular necrosis. Our second presentation used alveolar organoid systems derived from donor or IPF lung epithelial cells to demonstrate LTI-03's potential to promote and sustain type 2 alveolar epithelial cell, or AEC2, viability in the IPF lung as well as its ability to support AEC2 to type 1 alveolar epithelial cell, or AEC1, differentiation. We continue to be encouraged by the body of evidence supporting the potential of LTI-03 to treat IPF, for which novel treatment options are needed. These findings are in line with the promising data that we reported from the Phase 1b trial of LTI-03 in IPF, and we look forward to sharing topline interim data from our recently initiated Phase 2 RENEW IPF trial in the first half of next year." The first poster, entitled, "Pre-clinical Proof-of-concept of Anti-fibrotic Activity of Caveolin-1 Scaffolding Domain Peptide LTI-03 in Ex Vivo Precision Cut Lung Slices (PCLS) from Patients with Idiopathic Pulmonary Fibrosis," evaluates the antifibrotic effects of LTI-03, Rein's novel, multi-pathway, Caveolin-1 (Cav1)-related peptide currently in a Phase 2 trial for the treatment of IPF, and of nintedanib, a current standard of care treatment for IPF, in PCLS from 12 patients with end-stage disease. The PCLS samples were treated every 12 hours with one of 0.5 μM, 3.0 μM or 10.0 μM of LTI-03; 0.1 μM or 10.0 μM of nintedanib; or 10.0 μM of placebo, for five to seven days. Key Takeaways LTI-03 broadly attenuated profibrotic transcripts and proteins and the corresponding pathways of these factors, further supporting LTI-03's ability to inhibit profibrotic signaling. LTI-03 dose-dependently stimulated production of solRAGE, a factor indicative of AEC1 health that is a critically important aspect of IPF and has gone largely unaddressed by current treatment options. LTI-03 reduced the expression of profibrotic proteins in IPF PCLS, including Col-1α1 and platelet-derived growth factor receptor beta (PDGFRB). Unlike nintedanib, LTI-03 did not induce cellular necrosis or apoptosis. The second poster, entitled, "Evaluating Alveolar Regenerative Properties of Caveolin Scaffolding Peptides (CSD) in Three Dimensional (3D) Alveolospheres from IPF and Normal Donor Lung Samples," further explores the effects of LTI-03 and nintedanib on AEC2s in the normal and IPF lung. In these studies, the effects of LTI-2355, Rein's second generation Cav1-related peptide that is in preclinical development, were also examined. Eight (8) IPF lung explants and 10 normal donor lungs were processed to obtain lung epithelial cell preparations, from which AEC2s were isolated for lung organoid generation. Previous studies completed by Rein and others indicate that there is a significant decrease in the abundance of AEC2s in the IPF lung as compared to a normal lung, in turn impairing AEC2 to AEC1 differentiation and alveolar regeneration. The AEC2s from IPF and normal lung organoids were treated with 0.5 μM, 3.0 μM or 10.0 μM of either LTI-03, LTI-2355 or placebo, or 80.0 nM of nintedanib. Treatments were refreshed every other day in these lung organoid cultures for up to 28 days. Key Takeaways Cav1 scaffolding domain peptides LTI-03 or LTI-2355 sustained AEC2s in IPF lung organoids or alveolospheres, further supporting LTI-03's ability to promote alveolar epithelial cell survival. At the 10.0 μM dose, both LTI-03 and LTI-2355 increased the size of IPF alveolospheres compared to placebo at Day 28. Both LTI-03 and LTI-2355 appeared to protect normal lung alveolopheres, while nintedanib demonstrated significant growth-inhibiting or toxic effects on normal donor lung organoids at Day 28. About IPF IPF is a chronic lung disease characterized by progressive tissue scarring that prevents proper lung function. It is a progressive, fatal, age-associated lung disease affecting approximately 100,000 people in the United States1. IPF typically presents in adults 65 or older and is usually fatal within two to five years after diagnosis2. About LTI-03 and Caveolin-1 (Cav1) LTI-03 is a seven amino acid peptide, the sequence of which is derived from the caveolin scaffolding domain (CSD), an important binding region of the Cav1 protein. Cav1 normally serves a critical function in the prevention of fibrosis by maintaining a balance between pathways that both initiate and arrest lung repair and cell movement. Through the CSD, caveolin interacts with multiple signaling molecules, all of which possess a caveolin binding domain region. Cav1 expression is decreased in IPF lung tissues and has been demonstrated to decrease during the fibrotic phase of bleomycin, or BLM, lung injury in mice. Restoring the balance of important biological signals in the lung may not only slow lung function decline but could also restore healthy lung function through the protection of healthy epithelial cells. About Rein Therapeutics Rein Therapeutics is a clinical-stage biopharmaceutical company advancing a novel pipeline of first-in-class therapies to address significant unmet medical needs in orphan pulmonary and fibrosis indications. Rein's lead product candidate, LTI-03, is a novel, synthetic peptide with a dual mechanism targeting alveolar epithelial cell survival as well as inhibition of profibrotic signaling. LTI-03 has received Orphan Drug Designation in the U.S. A Phase 2 clinical trial of LTI-03 for the treatment of idiopathic pulmonary fibrosis was initiated in May 2025. Rein's second product candidate, LTI-01, is a proenzyme that has completed Phase 1b and Phase 2a clinical trials for the treatment of loculated pleural effusions. LTI-01 has received Orphan Drug Designation in the U.S. and E.U. and Fast Track Designation in the U.S. For more information, please visit the company's website at or follow them on LinkedIn and X. References1Pergolizzi, Jr., J., LeQuang, J., Varrassi, M., Breve, F., Magnusson, P., Varrassi, G., (2023). What Do We Need to Know About Rising Rates of Idiopathic Pulmonary Fibrosis? A Narrative Review and Update. Springer Nature, Published online 2023 Jan 24. Doi: 10.1007/s12325-022-02395-9.2Nathan et al. "Long-term Course and Prognosis of Idiopathic Pulmonary Fibrosis in the New Millennium". Chest Journal Volume 140, ISSUE 1, P221-229, July 2011. Forward-Looking Statements This press release may contain forward-looking statements of Rein Therapeutics, Inc. ("Rein", the "Company", "we", "our" or "us") within the meaning of the Private Securities Litigation Reform Act of 1995, including statements with respect to: the RENEW Phase 2 clinical trial of LTI-03, including with respect to the timing of the trial and the assumption that the Company will raise the funds necessary to conduct the trial; the therapeutic potential of LTI-03 and LTI-2355; and future expectations, plans and prospects for the Company. We use words such as "anticipate," "believe," "estimate," "expect," "hope," "intend," "may," "plan," "predict," "project," "target," "potential," "would," "can," "could," "should," "continue," and other words and terms of similar meaning to help identify forward-looking statements, although not all forward-looking statements contain these identifying words. Actual results may differ materially from those indicated by such forward-looking statements as a result of various important factors, including risks and uncertainties related to: the ability of the Company to obtain the cash resources to fund the RENEW Phase 2 trial through its completion and the Company's operations for the anticipated periods and the Company's ability to manage unplanned cash requirements; changes in applicable laws or regulations; the possibility that the Company may be adversely affected by other economic, business, and/or competitive factors, including risks inherent in pharmaceutical research and development, such as adverse results in the Company's drug discovery, preclinical and clinical development activities; the risk that the results of preclinical studies and early clinical trials may not be replicated in later clinical trials, including in the RENEW Phase 2 trial, or that partial results of a trial will be indicative of the full results of the trial; the Company's ability to enroll patients in its clinical trials; and the risk that any of its clinical trials may not commence, continue or be completed on time, or at all; the Company's ability to successfully integrate Qureight Ltd.'s deep-learning platform into the RENEW Phase 2 trial; decisions made by the U.S. Food and Drug Administration and other regulatory authorities, investigational review boards at clinical trial sites and publication review bodies with respect to our development candidates; as well as the risks and uncertainties discussed in the "Risk Factors" section of the Company's Annual Report on Form 10-K for the year ended December 31, 2024, which is on file with the United States Securities and Exchange Commission (the "SEC") and in subsequent filings that the Company files with the SEC. These forward-looking statements should not be relied upon as representing the Company's view as of any date after the date of this press release, and we expressly disclaim any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. Rein Investor Relations & Media Contact:Argot Partnersrein@ View original content to download multimedia: SOURCE Rein Therapeutics, Inc. Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Yahoo
13-05-2025
- Business
- Yahoo
Rein Therapeutics begins trial for idiopathic pulmonary fibrosis treatment
Rein Therapeutics has initiated the randomised RENEW Phase II trial of its Caveolin-1-related peptide, LTI-03, targeting idiopathic pulmonary fibrosis (IPF), with subject screening and recruitment now underway. The double-blind, placebo-controlled, multi-centre trial is designed to assess the tolerability, efficacy and safety of LTI-03 in IPF patients. Additionally, it will evaluate the inhaled dry powder LTI-03 activity across various biomarkers and measure lung function, and the potential for regeneration of healthy tissue. It aims to enrol nearly 120 subjects who have been diagnosed with this condition within five years of screening. These subjects may also be receiving standard-of-care antifibrotic treatment. The study will span up to 50 sites worldwide, including Germany, the US, Austria, Poland, and the UK. Rein noted that subjects in the trial will be randomised into two blinded placebo-controlled cohorts. In the low dose cohort, subjects will be given 2.5mg of either the therapy or placebo, administered two-times daily for a total daily dose of 5mg. The high-dose cohort will be given 5mg twice a day, totalling 10mg per day. Rein Therapeutics president and CEO Brian Windsor said: "Following productive FDA interactions and positive topline results from the Phase Ib trial, we have designed our RENEW trial to test the promise of our dual mechanism approach to targeting alveolar epithelial cell survival and the inhibition of profibrotic signalling in this patient population.' The incidence of treatment-emergent adverse events from day one through week 24 is the primary endpoint of the trial. The key secondary endpoint is the efficacy of the therapy, which will be measured via percent predicted FVC, forced vital capacity and computer tomography, in partnership with Qureight. Subjects will undergo a screening period for 28 days before randomisation and a 24-week treatment duration, with a follow-up period of four weeks. Previously, the company reported positive top-line outcomes from cohort two of the Phase Ib trial of the therapy in IPF, where a positive trend was identified in seven out of eight biomarkers assessed. Five biomarkers showed dose-dependent effects, and four met statistical significance when combining data from cohorts one and two. "Rein Therapeutics begins trial for idiopathic pulmonary fibrosis treatment" was originally created and published by Clinical Trials Arena, a GlobalData owned brand. The information on this site has been included in good faith for general informational purposes only. It is not intended to amount to advice on which you should rely, and we give no representation, warranty or guarantee, whether express or implied as to its accuracy or completeness. You must obtain professional or specialist advice before taking, or refraining from, any action on the basis of the content on our site. Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
