Wednesday, January 9, 2019
Masimo sees FY19 adjusted EPS $3.05, consensus $3.04
Sees product revenue increasing to $910M, which reflects reported growth of 9.6% to 10% and constant currency growth of 10.5% to 10.9%; Includes approximately $7M of year-over-year currency headwinds in revenue guidance. Revenue consensus $906.52M.
https://thefly.com/landingPageNews.php?id=2846203
DaVita price target lowered to $65 from $78 at RBC Capital
RBC Capital analyst Frank Morgan lowered his price target on DaVita to $65 and also reduced his FY19 EPS view to $3.93 from $4.12 after its management provided initial FY19 operating income outlook of $1.54B-$1.64B relative to consensus of $1.62B. The analyst notes that the company’s near term is likely to be impacted by “industry headline risk, potential margin pressures due to increased scrutiny of dialysis rates, and ongoing labor cost growth”, but sees dialysis as a “steady, stable, defensive industry over the long term, with predictable patient volumes and strong cash flows”.
https://thefly.com/landingPageNews.php?id=2846249
Intuitive Surgical reports preliminary Q4 revenue $1.05B, consensus $1.03B.
https://thefly.com/landingPageNews.php?id=2846258
Tuesday, January 8, 2019
Rituximab beneficial in secondary progressive MS
For patients with secondary progressive multiple sclerosis (SPMS), treatment with rituximab is associated with a significantly lower Expanded Disability Status Scale (EDSS) score and delayed progression, according to a study published online Jan. 7 in JAMA Neurology.
Yvonne Naegelin, M.D., from the University of Basel in Switzerland, and colleagues conducted a retrospective cohort study using data from patients with SPMS at three multiple sclerosis centers from 2004 to 2017. The EDSS score was compared for 54 patients with SPMS treated with rituximab and 59 patients not treated with rituximab; after propensity score matching, 44 pairs of patients were included. Patients were followed for up to 10 years.
The researchers found that patients with SPMS who were treated with rituximab had a significantly lower EDSS score during a mean follow-up of 3.5 years in the covariate-adjusted matched set (mean difference, −0.52). In the rituximab-treated group, the time to confirmed disability progression was significantly delayed (hazard ratio, 0.49).
"Only a few anti-inflammatory treatments may be associated with a beneficial outcome in patients with SPMS," the authors write. "The differential response to these treatments may provide clues to understanding which parts of the B-cell response are pathogenic in SPMS and which patients might benefit from such treatments."
Several authors disclosed financial ties to pharmaceutical companies, including Biogen, which manufactures rituximab.
The researchers found that patients with SPMS who were treated with rituximab had a significantly lower EDSS score during a mean follow-up of 3.5 years in the covariate-adjusted matched set (mean difference, −0.52). In the rituximab-treated group, the time to confirmed disability progression was significantly delayed (hazard ratio, 0.49).
"Only a few anti-inflammatory treatments may be associated with a beneficial outcome in patients with SPMS," the authors write. "The differential response to these treatments may provide clues to understanding which parts of the B-cell response are pathogenic in SPMS and which patients might benefit from such treatments."
Several authors disclosed financial ties to pharmaceutical companies, including Biogen, which manufactures rituximab.
More information: Abstract/Full Text (subscription or payment may be required)
https://medicalxpress.com/news/2019-01-rituximab-beneficial-secondary-ms.html
Histamine can boost long-term memory of objects
Allergy sufferers may use antihistamines to reduce symptoms, but new research reveals that better long-term memory might be possible with pro-histamine treatment. Long-term memory is used to remember anything before 48 hours ago.
During recent studies by researchers in Japan, histamine improved people’s long-term memorytest scores depending on the strength of the original memory, and could temporarily extend micememories by as much as 25 days longer than normal. Clarifying the role of histamine in memory may alleviate symptoms of memory disorders such as Alzheimer’s disease and other forms of dementia.
Professor Yuji Ikegaya and lecturer Hiroshi Nomura, Ph.D., of the University of Tokyo led a research team that included collaborators at Hokkaido University and Kyoto University in Japan.
A total of 38 men and women in their mid-20s completed memory tests over three days. Participants looked at pictures of familiar objects, like eyeglasses or a wristwatch, and then several days later, were shown some of the same images, as well as some similar and some new photos, and were asked if they had seen the image before.
“In real life, we cannot know what we forgot. This is why we do human memory tests with pictures on a computer screen,” said Ikegaya.
Seven or nine days later, participants were given either a placebo or a large dose of a medication that increases the amount of histamine in the brain. The unusually large dose ensured the medication crossed the blood-brain barrier, the body’s natural defense that inhibits entry into the brain. The same medication is normally prescribed at lower doses to treat dizziness.
Duality
After taking the drug, participants with poor memories recognized more images correctly, while images that had been difficult to recall became easier for all participants to recognize. However, taking the drug lowered scores of participants with good memories, and images that had been easier to recall became slightly more difficult for all participants to recollect.
“To any students thinking about using this drug as a study aid, I must warn them to first always protect their health, and second to realize that we have not tested whether this drug helps anyone learn or memorize new things,” said Ikegaya.
“Increased histamine helped research participants remember an image they knew once but couldn’t remember during a long-term memory word-association test,” said Ikegaya.
Researchers suspect that the phenomenon of stochastic resonance, adding white noise to a transmission to boost signal strength, may cause the dual effect of histamine improving long-term memory sometimes but hindering it at other times.
Histamine threshold
Ikegaya suggests memory is a combination of a gradient system and a yes:no or 1:0 digital system. Information might be stored in the brain as a gradient, but nerves do not fire until they are above a particular threshold. Below this threshold is “no” or 0, and we cannot remember. Above this threshold is “yes” or 1, and we can remember.
“You still have the memory, but you can’t access it unless it is above a particular threshold,” said Ikegaya.
Researchers suspect that the drug raises the histamine gradient to the point that the neurons involved in the latent memory reach the threshold level required to fire a signal and make us remember. However, for memories already over the threshold naturally, extra histamine adds too much noise and excessive nerve signaling hinders recall.
Histamine had no effect on participants’ scores on tests unrelated to long-term memory.
Mouse memories
Researchers gave mice two plastic toys, one the mice had seen before and another that was new. Mice prefer to explore a new toy, but after three days, mice forget and treat all toys as new. After receiving a medication that increases histamine in the brain, mice could recognize toys they’d seen as long as 28 days ago.
The long-term memory boost was temporary, though. On day 29, all toys were new again to the mice. Researchers saw similar results with two drugs that increase histamine: thioperamide and betahistine.
Experiments to examine the activity of individual neurons in mouse brains revealed that the drugs increased histamine specifically in a brain region known to be involved in visual perception and memory, called the perirhinal cortex. Moreover, histamine reactivated the same neurons that were active in making the memory.
Bad memories
Improved long-term memory is not always beneficial, such as for sad or fearful memories, or in disorders such as post-traumatic stress disorder (PTSD). Remembering and forgetting are not simple opposites. Instead, researchers suspect that different brain regions and processes are involved in remembering and forgetting.
“If we have typical memory, then there is a balance between the brain systems for remembering and for forgetting. Too much forgetting or too much remembering is likely an upset of that balance,” said Ikegaya.
Future memories
Researchers are currently planning future studies to test how histamine levels might affect memory test results in older adults. Other studies will also examine how histamine might be involved in prospective memory, the “don’t forget”-type of memories for the future, such as things we might write on reminder sticky notes to our future selves.
This research published in the journal Biological Psychiatry is peer-reviewed and included experimental studies in mice and small-scale randomized control trials in people. The neurotransmitter histamine affects the immune response, memory and acid levels in the stomach. Specialized receptors in different areas of the body regulate the different functions of histamine.
Explore further
More information: Hiroshi Nomura et al. Central histamine boosts perirhinal cortex activity and restores forgotten object memories. 8 January 2019. Biological Psychiatry. DOI: 10.1016/j.biopsych.2018.11.009
Hormone could slow Alzheimer’s progression
Queen’s University researcher Fernanda De Felice (Psychiatry), along with co-authors from the Federal University of Rio de Janeiro, have identified an exercise-linked hormone that could slow the progression of Alzheimer’s disease. This research was recently published in the high-profile publication, Nature Medicine.
The findings show that irisin, a hormone that is boosted by exercise, plays an important role in the brain and that Alzheimer patients carry less of the hormone. This discovery moves scientists one step closer to developing a medication that reproduces the effects of exercise-induced irisin production in the brain.
“In the past few years, researchers from many places around the world have shown that exercise is an effective tool to prevent different forms of dementia such as Alzheimer’s” says Dr. De Felice, a researcher in the Centre for Neuroscience Studies at Queen’s. “This has led to an intense search for specific molecules that are responsible for the protective actions of exercise in the brain. Because irisin seems to be powerful in rescuing disrupted synapses that allow communication between brain cells and memory formation, it may become a medication to fight memory loss in Alzheimer’s disease.”
The new research is important, explains Dr. De Felice, because curing dementia is one of the greatest current and future health care challenges. Unfortunately, despite 30 years searching for treatment drugs, there is no effective medication for Alzheimer’s disease. She adds it is also important to remember that the vast majority of patients with dementia can be disabled due to other age-related illness (e.g. arthritis, heart disease, obesity, visual problems, and depression). Furthermore, it can be challenging to engage a patient in regular physical activity.
A drug that increases irisin in the brain could be the key.
“It is important to keep in mind that Alzheimer’s is a very complex disease and it is truly hard to treat Alzheimer’s patients before irreversible damage occurs in their brains. This is because when a patient is diagnosed with Alzheimer’s disease, their brain has already been damaged,” Dr. De Felice says. “Finding new protective routes, such as the identification of an exercise-linked component, may be an optimal strategy to heal the brain before brain cells die and dementia becomes irreversible.”
The next step in Dr. De Felice’s research is investigating the most effective way of delivering irisin to the brain.
Explore further
More information: Mychael V. Lourenco et al. Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models, Nature Medicine (2018). DOI: 10.1038/s41591-018-0275-4
Where Are They Now? Top 3 Biotech Startups From NextGen Bio Class of 2015
Every year, BioSpace analyzes the biotech industry, looking for the hot new biotech startups to watch. We then produce the NextGen Bio “Class of…,” twenty companies ranked based on several categories, including Finance, Collaborations, Pipeline, and Innovation. The companies were typically launched no more than 18 months before the list was created.
We thought it would be insightful to look back at our previous lists to see where some of those companies are today. Here’s a look at the top 3 companies from the Top 30 Life Science Startups to Watch in the U.S. from 2015. Yes, in 2015 we chose 30, but since then the count has been 20.
#1. Juno Therapeutics. Founded in 2013, Juno Therapeutics was our top pick for the NextGen Bio Class of 2015. At that time, Juno was noted for partnerships with Fred Hutchinson Cancer Research Center, the Memorial Sloan-Kettering Cancer Center, and Seattle Children’s Research Institute. The initial Series A investment was $120 million followed in April 2014 by a secondary Series A with an additional $176 million. Not long afterward, in August 2014, Juno closed on a Series A and B round worth $134 million, bringing in more than $300 million in less than 12 months. It launched its initial public offering on December 23, 2014, raising another $100 million.
What had investors—wisely—excited about Juno was its novel cellular immunotherapies based on two separate but complementary platforms—Chimeric Antigen Receptors (CARs) and T Cell Receptors (TCRs). The company had its share of setbacks. In March 2017 it had to shutter its lead CAR-T oncology program, JCAR015, because of patient deaths. But it bounced back with JCAR017.
Then, you could say, lightning struck. In January 2018, Celgene acquired Juno for $9 billion. Juno was keeping its name and operating as a wholly-owned subsidiary of Celgene and also staying at its location.
In June 2018, at the Annual Meeting of the American Society of Clinical Oncology (ASCO), Juno presented research for JCAR017 (lisocabtagene maraleucel) in diffuse large B-cell lymphoma (DLBCL), the most common form of non-Hodgkin’s lymphoma (NHL). The results were very positive, and and the product has the potential of becoming only the third CAR-T therapy on the market. Multiple clinical trials are in progress.
#2. MyoKardia. Based in San Francisco, MyoKardia was second on the list for 2015. The company had raised $52 million in three rounds from a single investor. In May 2014, it launched the Sarcomeric Human Cardiomyopathy Registry (ShaRe), a multi-center, international repository of clinical data on individuals with genetic heart disease. And in September 2014, it inked a deal with Sanofi to collaborate on discovering and developing first-of-its-kind targeted therapeutics for heritable heart diseases known as cardiomyopathies. This collaboration provided up to $200 million in equity investments, milestone payments and R&D services through 2018.
MyoKardia’s lead program is for Mavacamten, an orally administered small molecule designed to reduce left ventricular contractility by modulating the function of cardiac myosin. It is currently being evaluated in EXPLORER, a Phase III open-label single-arm study in patients with symptomatic oHCM, a subset of hypertrophic cardiomyopathy (HCM).
The company also has another Phase II product, MYK-491, for dilated cardiomyopathy. The company also has other compounds in preclinical development related to the treatment of cardiac muscle contractility in HCM.
#3. Spark Therapeutics. Based in Philadelphia, Pa., Spark Therapeutics was launched in 2013 with a $50 million capital commitment from The Children’s Hospital of Philadelphia (CHOP) to advance and commercialize its ongoing gene therapy programs, including its lead candidate for RPE65-related blindness, which at that time was in Phase III clinical trials. The company raised $122.8 million in two rounds. It also at that time had a Phase I and II program in hemophilia B.
In December 2017, the U.S. Food and Drug Administration (FDA) approved Spark’s Luxturna (voretigene neparvovec), a gene therapy for a rare, genetic form of blindness. It is the first type approved by the FDA that targets a disease caused by mutations in a specific gene. It was approved for the treatment of pediatric and adult patients with confirmed biallelic RPE65 mutation-associated retinal dystrophy. The disease can lead to vision loss and may cause complete blindness in certain patients.
In what stunned many, the therapy came with an $850,000 price tag to treat both eyes. That price was actually at the low end for many analysts, who expected it to be close to $1 million, or $500,000 per eye. Still, that made the drug the most expensive therapy in the United States. The disease affects between 1,000 and 2,000 patients in the United States.
Part of the price and part of the reason payors, such as Harvard Pilgrim, an affiliate of Express Scripts, were willing to pay for it was an agreed-upon outcomes-based payment system and a payment system. In January 2018, Steve Miller, chief medical officer for Express Scripts, told CNBC that the drug was responsibly priced. “The product is just phenomenally innovative, and we’ve been talking about gene therapy for over 20 years. We’re now at the threshold of having gene therapy reaching patients,” he said.
The therapy was recently approved in Europe. The company is also preparing for a Phase III trial of SPK-8011 for hemophilia A before the end of this year and hopes to get an investigational gene therapy for Pompe disease into the clinic in 2019.
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