Category Archives: Neurology

Summit Therapeutics to expand clinical trials after healthy interim results

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Summit Therapeutics will expand enrollment in its phase 2 clinical trials studying the effect of ezutromid treatment on Duchenne muscular dystrophy (DMD), the company said on Wednesday.

The PhaseOut DMD trial is a multi-centre, 48 week open-label clinical trial with 40 enrolled patients between the ages of five and ten who suffer from DMD which will be enhanced by the newly announced parallel running expansion.

David Roblin, chief operating and medical officer of Summit, said: “We are extremely grateful to the patients who participated in our Phase 1 clinical trials and contributed to ezutromid’s clinical advancement, but were not initially eligible to participate in our Phase 2 clinical trial. Accordingly, we are pleased to open this additional group in our Phase 2 and provide these patients with the opportunity to receive ezutromid treatment.”

Patients with DMD will be eligible for the expanded trial regardless of their age or ambulatory status.

DMD is a muscle wasting disease that affects approximately 50,000 men and boys in the developed world and is caused by genetic faults in the gene that codes dystrophin and thus preventing the healthy function of all muscles.

The orally administered small molecule drug is intended to modulate utrophin, a protein functionally and structurally similar to dystrophin, with the aim of slowing or even halting DMD.

Recently announced 24 week interim data from the trials demonstrated that compared to baseline, ezutromid significantly reduced muscle damage and muscle inflammation attributed to the disease.

“We expect the data collected from this additional group of patients will help expand our understanding of ezutromid’s safety and efficacy profile across a broader patient population,” said Roblin.

Ezutromid has been granted Fast Track designation and Rare Pediatric Disease designation by the US Food and Drug Administration (FDA) as well as orphan drug status which allows for additional regulatory support and a period of market exclusivity following approval.


How thalidomide is effective against cerebral infarction

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Scientists reveal that this dangerous drug could suppress nerve cell death.

Notoriously remembered as a major pharmaceutical scandal approximately 60 years ago, thalidomide caused severe birth defects when many pregnant women took the drug as a remedy for their morning sickness.

In recent years, however, thalidomide and its derivatives have been widely used to treat haematologic malignancies such as multiple myeloma.

Evidence also suggests that thalidomide has a neuroprotective effect, reducing both oxidative stress and inflammatory response, but the exact molecular mechanisms of thalidomide on the brain were unknown.

To investigate, scientists at Waseda University and Tokyo University of Pharmacy and Life Sciences studied thalidomide’s target protein, cereblon (CRBN), and its binding protein, AMP-activated protein kinase (AMPK), which plays an important role in maintaining intracellular energy homeostasis in the brain.

Through their study, they revealed that thalidomide inhibits the activity of AMPK via CRBN under oxidative stress and suppresses nerve cell death.

“We hope that our findings will help with the development of new and safer thalidomide derivatives,” says Naoya Sawamura, Associate Professor of Neuropharmacology at Waseda University and leading author of this study, “to better treat diseases such as cerebral infarction, a type of stroke, which is a major cause of death worldwide.”

Specifically, Sawamura’s research group used cerebral ischaemia model rats of the cerebral artery occlusion/reperfusion (MCAO/R) to examine the effect of thalidomide on infarct lesions caused by cerebral ischaemia and related intracellular signals.

After performing qualitative analysis and assessments on the rats’ physical movements, they found that thalidomide treatment significantly decreased the infarct volume and neurological deficits in MCAO/R model rats, and that AMPK was the key signalling protein in the mechanism through additional experiments.

Moreover, to determine the molecular mechanisms of the effect of thalidomide on neuronal death, they used oxidative stress-induced neuronal cells, which were induced by administration of H2O2, as cerebral ischaemia model cells.

“In these cells, we found that the AMPK-CRBN interaction weakened and phosphorylation of AMPK enhanced, but thalidomide treatment restored the AMPK-CRBN interaction and suppressed phosphorylation of AMPK,” explains Sawamura.

“What this implies is that thalidomide regulates AMPK-CRBN interactions in cells under ischaemic conditions, meaning, it can suppress nerve cell death.”

Further study is needed to identify effective thalidomide derivatives with fewer side-effects, as well as more stability because they undergo hydrolysis spontaneously and rapidly in aqueous solutions.

Nevertheless, Sawamura is excited about the future possibilities of this study.

“Our attention is now on the functions of CRBN as a stress response molecule. The suppression of nerve cell death by thalidomide perhaps occurs because CRBN’s function as a stress molecule is somehow enhanced.”

“We want to elucidate the response of cereblons in ageing and stress models to see if decline in the CRBN function could be a biomarker for ageing and stress.”


Migraine maven Lilly finds ‘understanding gap’ between patients, nonpatients in new survey

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Disconnects still exist in perceptions around migraines.

Surveying both migraine sufferers and average consumers, Eli Lilly found significant understanding gaps between the two.

For instance, migraine patients estimated their pain episodes lasted an average of 31 hours, while nonsufferers guessed the average fell around 21 hours. Migraine patients also rated the pain they felt much higher than the average person’s rating of what they imagined the pain to be.

“There is a huge stigma in migraine,” said Sheena Aurora, a physician who has treated migraine patients and is now a medical fellow at Eli Lilly. “… Sometimes even people with migraines don’t realize the impact of their disease. When I treated patients with migraines, I would ask them how many migraine headache days did they have, and they would have to stop and think about it.”

Lilly undertook the survey to determine migraine perceptions among three groups of people: migraine sufferers, caregivers and loved ones, and consumers who didn’t know anyone who suffers from migraines.

Other poll findings included that migraine patients feel stressed and that they’re missing out on life. Patients reported that migraines had prevented them from doing what they wanted in their lives for an average 7 days out of the previous 30 days.

During the previous year, the migraines had been severe enough to force them to miss an average of 7.4 important events, such as birthday or holiday gatherings. And an overwhelming majority—82%—agreed that it is stressful to have an unpredictable disease like migraine.

“By highlighting their unmet needs and continuing to do that, then we can help patients talk to their physicians, help physicians recognize their impact and perhaps even help payers understand the impact of migraines,” Aurora said.

She noted that the survey and other studies around migraines are important as new treatments created specifically for migraines come to market. Of the four currently FDA-approved drugs, none were designed exclusively for migraines, a fact that is often seen in low adherence when patients can’t take the side effects or don’t get enough relief, Aurora said.

Lilly is currently working to bring a new class of migraine therapy to market. The Indianapolis drugmaker has already filed a Biologics License Application with the FDA for its CGRP inhibitor maintenance drug galcanezumab, which is eventually expected to go up against contenders from companies including Amgen and Teva.

Meanwhile, Lilly’s first-in-class acute migraine candidate lasmiditan is in late-stage trials with expectations for FDA filings this year.


Study finds antidepressants to be more effective than placebos

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Major international study – comprising largest amount of unpublished data to date – has found that antidepressants are more effective than placebos for short-term treatment of acute depression in adults.

Meta-analysis of 522 trials compared 21 commonly used antidepressants and concluded all of them to be more effective than placebos for the short-term treatment of acute depression in adults, with effectiveness ranging from small to moderate for different drugs.

The trials analysed were all double-blind, randomised controlled trials (RCTs) with a total of 116,477 participants. The study includes the largest amount of previously unpublished data to date, all of which is now freely available online.

“Our study brings together the best available evidence to inform and guide doctors and patients in their treatment decisions. We found that the most commonly used antidepressants are more effective than placebos, with some more effective than others. Our findings are relevant for adults experiencing a first or second episode of depression – the typical population seen in general practice.” says lead author Dr Andrea Cipriani, University of Oxford and the NIHR Oxford Health Biomedical Research Centre.

Antidepressants can be an effective tool to treat major depression, but this does not necessarily mean that antidepressants should always be the first line of treatment.

“Medication should always be considered alongside other options, such as psychological therapies, where these are available. Patients should be aware of the potential benefits from antidepressants and always speak to the doctors about the most suitable treatment for them individually,” Ciprianiconcludes.

Large-scale worldwide illness

An estimated 350 million people have depression worldwide. The economic burden in the USA alone has been estimated at more than US$210 billion. Pharmacological and non-pharmacological treatments are available but owing to inadequate resources, antidepressants are more frequently used. However, there is considerable debate about their effectiveness.

As part of the study, the authors identified all double-blind RCTs that compared antidepressants with placebos, or with another antidepressant (head-to-head trials) for the acute treatment (over eight weeks) of major depression in adults aged 18 years or more. The authors then contacted pharma companies, original study authors, and regulatory agencies in order to supplement incomplete reports of the original papers, or provide data for unpublished studies.

Researchers use data mining to expedite effective prescriptions for depression patients…

The primary outcomes were efficacy (number of patients who responded to treatment, ie who had a reduction in depressive symptoms of 50% or more on a validated rating scale over eight weeks) and acceptability (proportion of patients who withdrew from the study for any reason by week eight).

Overall, 522 double-blind RCTs carried out between 1979 and 2016 that compared 21 commonly used antidepressants or placebos were included in the meta-analysis; the largest ever in psychiatry. A total of 87,052 participants had been randomly assigned to receive a drug, and 29,425 to receive placebos. The majority of patients had moderate-to-severe depression.

All 21 antidepressants were more effective than placebos and only one drug (clomipramine) was less acceptable than placebo.

Antidepressants effective to varying degrees

Some antidepressants were more effective than others, with agomelatine, amitriptyline, escitalopram, mirtazapine, paroxetine, venlafaxine, and vortioxetine proving most effective, and fluoxetine, fluvoxamine, reboxetine, and trazodone being the least effective. The majority of the most effective antidepressants are now off patent and available in generic form.

Antidepressants also differed in terms of acceptability, with agomelatine, citalopram, escitalopram, fluoxetine, sertraline, and vortioxetine proving most tolerable, and amitriptyline, clomipramine, duloxetine, fluvoxamine, reboxetine, trazodone, and venlafaxine being the least tolerable.

The authors note that the data included in the meta-analysis covers eight weeks of treatment, so may not necessarily apply to longer term drug treatment. The differences in efficacy and acceptability between different antidepressants were smaller when data from placebo-controlled trials were also considered.

Effects may not extend to bipolar condition

In order to ensure that the trials included in the meta-analysis were comparable, the authors excluded studies with patients who also had bipolar depression, symptoms of psychosis or treatment resistant depression, meaning that the findings may not apply to these patients.

“Antidepressants are effective drugs, but, unfortunately, we know that about one third of patients with depression will not respond. With effectiveness ranging from small to moderate for available antidepressants, it’s clear there is still a need to improve treatments further,” adds Dr Cipriani, .

Nothing is perfect

78% of the 522 trials were funded by pharma companies, and the authors retrieved unpublished information for 52% of the trials included in the meta-analysis. Overall, 9% of the trials were rated as high risk of bias, 78% as moderate, and 18% as low. The design of the network meta-analysis and inclusion of unpublished data is intended to reduce the impact of individual study bias as much as possible. Although this study included a significant amount of unpublished data, a certain amount could still not be retrieved.

“Antidepressants are routinely used worldwide yet there remains considerable debate about their effectiveness and tolerability. By bringing together published and unpublished data from over 500 double blind randomised controlled trials, this study represents the best currently available evidence base to guide the choice of pharmacological treatment for adults with acute depression. The large amount of data allowed more conclusive inferences and gave the opportunity also to explore potential biases,” says co-author Professor John Ioannidis, from the Departments of Medicine, Health Research and Policy, Biomedical Data Science, and Statistics, Stanford University, USA.

The international study was published in The Lancet.


Nusinersen improves motor function of children with SMA

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Clinical trial shows treatment is effective for children with spinal muscular atrophy.

Children with later-onset spinal muscular atrophy (SMA) were more likely to show gains in motor function when treated with a new medication compared to children receiving a sham procedure, according to a new study. The study demonstrates the impact the drug, nusinersen, can have on older patients with this progressive neuromuscular disorder.“This treatment is transformative for the entire SMA community,” said Dr Richard S. Finkel, the Chief of Neurology at Nemours Children’s Hospital in Orlando and the senior author of the study. “One thing we have learned, though, is that the closer to symptom onset that children begin treatment, the more substantial the improvement in motor function. However, even with delayed use, we observed significant improvements in older children with SMA on nusinersen.”

SMA is classified based on the age at symptom onset, as well as the most advanced motor milestone attained during development. Past studies have evaluated the safety of nusinersen in SMA Type 1, the most severe form that affects infants, usually before six months of age and who do not achieve sitting. Children with SMA Type 2 experience symptoms after six months of age and attain sitting before experiencing the muscle weakness and decline in motor function that are hallmarks of this genetic disease.

Before nusinersen, no targeted drug treatments were available for SMA. This treatment modifies the SMN2 gene with an antisense oligonucleotide (ASO), a tiny fragment of synthetic DNA, injected directly into the spinal fluid. The DNA gets absorbed into nerve cells of the spinal cord to increase production of a protein required for neuromotor development.

The researchers noted greater improvements in a motor function score in children treated with nusinersen for at least six months. In total, 57 percent of children in the nusinersen group had an increase of at least three points in functioning scores from the start of the trial to the end of the examination period, compared with 26 percent of patients in the control group that achieved the same level improvement.

The study, known as the CHERISH trial, enrolled 126 children ages 2 to 12 with SMA Type 2 in a multicenter, randomised, double-blind, sham-controlled study from November 2014 through February 2017 to determine the safety and efficacy of the drug in these older patients. Children were administered four doses over nine months, followed by a six-month examination period, before being invited to participated in an open-label extension study.

There are some limitations to the study, including the strict eligibility criteria, which enrolled a more homogeneous and younger group of patients than those in clinical practice. Participants were required to be able to sit independently at the start of the study, with no severe contractures or scoliosis, limited ventilation support, and no use of a gastric feeding tube.

The availability of an effective treatment has led Dr Finkel and colleagues to spearhead efforts to have SMA included in the Health Resources and Services Administration’s Recommended Uniform Screening Panel, a newborn screening panel of conditions that warrant immediate identification after birth. The panel has recently approved this recommendation and is awaiting signature by the head of Health and Human Services. If included, infants with SMA could be diagnosed routinely and treated before symptoms appear.

The study has been published in the New England Journal of Medicine.


Blood-based epigenetic may hold clues to autism

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Epigenetic data reveals immune-response pathways that may prove critical to understanding autism.

Using data from blood and brain tissue, a team led by researchers at Johns Hopkins Bloomberg School of Public Health found that they could gain insights into mechanisms that might help explain autism by analysing the interplay between genes and chemical tags that control whether genes are used to make a protein, called epigenetic marks.

The findings could ultimately help lead to new ways of treating and preventing the disorder.

To investigate this question, Dr Margaret Daniele Fallin, chair of the Bloomberg School’s Department of Mental Health and director of the School’s Wendy Klag Center for Autism and Developmental Disabilities and her colleagues started by surveying four different tissue types–blood and cord blood from their own collections, as well as lung and fetal brain tissue from public collections–to find small variations in the genetic code of each sample that appear to be responsible for DNA methylation state, a type of epigenetic modification, in that particular tissue.

The researchers examined millions of these genetic code variations, known as single nucleotide polymorphisms (SNPs) and found thousands that control DNA methylation in some or all tissue types. They then matched up these SNPs with those already known to be associated with autism and saw that more autism-associated genes act to control DNA methylation than would be expected by chance. This was true in both blood and fetal brain tissue.

When the researchers looked at the role of genes that were methylated by genes with code differences related to ASD, including additional genes beyond those with direct code changes, they found that the majority were involved in biological pathways that were important in immune function.

The finding wasn’t surprising, Dr Fallin explains–numerous studies have identified abnormal gene expression of immune genes in autism samples and environmental experiences such as prenatal infection or prenatal exposure to pollutants that can ramp up immune responses are risk factors for ASD. However, none of the genetic code mutations directly identified in autism had pointed to these pathways. It is only when considering which other genes they may regulate that this biology is revealed.

More study on these biological pathways, she says, could lead to specific genes or proteins that could be modifiable with pharmaceuticals or other interventions, possibly offering new ways to prevent or treat ASD.

Researchers have long known that chemical modifications, a collection of “marks” on DNA known as the epigenome, play a key role in how cells operate by guiding differences between various tissue types in a given individual’s body, despite the fact that they all carry the same genetic code.

“The reason a brain cell is different from a heart cell is because of the epigenome, which affects which parts of a cell’s DNA are read,” says study Dr Fallin. “Think of it like an encyclopedia with a bunch of tabs. Cells don’t need to read the entire encyclopedia; they jump to the tabs they need to get things done.”

The current work shows that changes in the genetic code of a particular gene can control epigenetic marks at different genes, implying that a gene’s genetic code can affect whether other genes are turned on and off, which makes it important to understand the function of all genes involved, not just the one with the so-called misspelling.

“Our findings suggest that looking only at genes with misspellings related to autism might be too narrow a focus,” said Dr Fallin. “Instead of looking solely at the genes directly implicated in autism through their genetic code changes, we really should be also studying the functions of the other genes implicated by these changes in genetic code through epigenetic connections. “

“We made our findings here by comparing brain data to blood data,” she says, “but the vast majority we could have learned from the blood.”


Eisai banks on potential of Biogen’s Alzheimer’s drug

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Drug developers investigating Alzheimer’s drugs know that they’re taking a gamble; there have been numerous big failures that have caused larger companies to shy away from the difficult-to-treat area.

Only recently, Axovant, a part of the “vant” group of companies that attempts to rescue out-of-favour drug candidates, revealed that its Alzheimer’s drug had failed, wiping off most of the value of the company.

However, Eisai has displayed serious confidence in Biogen’s Alzheimer’s treatment that could spark increased interest that the latter company may be onto something.

The move sees Eisai take up a licensing option agreed with Biogen in 2014, that will see them pick up some of the development costs of aducanumab in return for the ability to bring the drug to market in Asia, whilst also picking up specified percentages through the rest of the world.

The original 2014 deal saw Biogen and Eisai work together on developing two of the latter’s Alzheimer’s candidates, which Eisai saw receive the right to opt-in to develop and commercialise two of Biogen’s compounds.

The like-for-like deal had gone quiet until now, with Eisai deciding to take up the offer on aducanumab. Clearly Eisai has seen enough to think that opting is a gamble worth taking; it means that the two candidates Eisai had brought to the table, E2609 and BAN2401, will no longer yield any milestone payments for the company. However, neither will Eisai have to pay anything to gain access to co-develop aducanumab.

Biogen will continue to be the lead developer of the drug through ongoing Phase 3 trials, as well as shouldering the costs of developing it until April 2018. At which point, Eisai will take on 15% of the cost until the end of 2018 and will then cover 45% of the funding from January 2019 onwards.

Eisai CEO Haruo Naito commented, “Genetic epidemiological studies such as the Icelandic genetic research as well as the knowledge recently gained from various clinical studies such as the aducanumab Phase 1b trial have deepened our conviction in the amyloid hypothesis […] In accordance with this new paradigm, we plan to further co-develop the collaboration products and hope to advance the world’s potentially first new treatment for Alzheimer’s disease based on the amyloid hypothesis. Through the collaboration and by leveraging each company’s respective strengths in each region, we hope to maximize the benefits for patients and their families.”

As footnote to this deal, it was announced that co-promotion agreement was reached between the two companies in regards to Avonex, Tysabri and Tecfidera in Japan, India and other Asia-Pacific markets, excluding China.


Lundbeck and Otsuka start phase III for Rexulti in bipolar

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Otsuka and co-development partner Lundbeck have started two phase III trials of their atypical antipsychotic Rexulti in bipolar disorder, potentially adding a third indication for the drug.

The two companies have started enrolling patients into the two studies, which will evaluate Rexulti (brexpiprazole) as a treatment for manic episodes in bipolar patients that are accompanied by depressive symptoms and require hospitalisation.

First approved in 2015, Rexulti is currently available as an adjunctive therapy for adults with major depressive disorder as well as for schizophrenia and after a slow start, has seen its sales growth accelerate, with Lundbeck reporting turnover of the drug up 85% to $91m in the first half of the year.

It has a long way to go however before it can reach the heights of its predecessor – Abilify (aripiprazole) – which was a mainstay for both Lundbeck and Otsuka but has fallen off the patent cliff in recent years and seen steep sales decline as a result, although a long-acting depot formulation (Abilify Maintena) is still making gains.

To date Rexulti has only been launched in the US, Canada and Australia, although it was filed for approval in Europe in schizophrenia earlier this year.

The partners recently suffered a big setback in their plans for brexpiprazole after the drug posted mixed results in agitation in Alzheimer’s disease patients, a condition that affects millions of people worldwide. They were hoping brexpiprazole could become the first antipsychotic to be approved in that indication, but while one trial was positive, a second failed to hit the mark, leaving the future of the programme in doubt. They also were unable to convince the FDA that the drug improved cognitive function in patients with depression.

Approval for bipolar patients would not have the same large-scale opportunity but could still add momentum to the new drug as it would mean brexpiprazole would match the indications of Abilify. Lundbeck and Otsuka are also evaluating the drug in a phase II trial involving patients with post-traumatic stress disorder (PTSD).

The bipolar trials are comparing brexpiprazole to placebo on their ability to improve Young-Mania Rating Scale (YMRS) scores, a widely-used clinician rating scale.

Rexulti is one of a string of new drugs at Lundbeck – along with Abilify and antidepressant Brintellix (vortioxetine) – which it is banking on to help it weather the loss of patent protection for Abilify and former blockbuster antidepressant Lexapro/Celexa (escitalopram).


Lupin scoops up women’s health specialist Symbiomix for $150 million

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The US arm of Mumbai’s Lupin Pharmaceuticals has announced that it is has acquired US-based gynaecologic treatment specialist Symbiomix Therapeutics for $150 million in a move to double down on its offerings in the women’s health market.

The deal comprises an upfront payment of $50 million in addition to a number of time-based and performance-based milestone payments, all funded from internal funds. “The acquisition of Symbiomix and Solosec franchise significantly expands Lupin’s branded women’s health specialty business, which is presently anchored by Methergine tablets,” the company said of the deal.

Solosec, Symbiomix’s key offering, is an oral granule treatment of bacterial vaginosis, approved by the FDA in September his year and expected to hit the market by mid-2018, with at least ten years of exclusivity in the US thanks to its designation as a Qualified Infectious Disease Product (QIDP).

“This transaction is an important milestone in the evolution of our specialty business and gives Lupin a new therapeutic to bring to obstetricians and gynaecologists to treat a serious health condition they see frequently in their practices,” commented Vinita Gupta, Chief Executive Officer of Lupin.

The move from Lupin represents a step forward in its drive to pursue expansion of its speciality drugs portfolio in the US, a strategy which has seen the company recently shift focus onto the areas of women’s health, paediatrics and neurology.



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Many people worry that robots and artificial intelligence will eliminate jobs, including those in health care.

But a little AI might not be unwelcome to people tired of waiting for test results or other improvements to their average experience at the doctor’s office. AI could speed up care, make medications more affordable and give patients more time with their doctors. Here are four ways machine learning is already changing health care.

Diagnose Alzheimer’s Earlier

When it comes to managing the progression of Alzheimer’s disease, early diagnosis is key. But spotting the nascent signs of this neurodegenerative condition is challenging, which means by the time a patient is diagnosed, he or she is already experiencing many of the debilitating symptoms, such as loss of memory and cognitive function.

Harnessing the power of Big Data could completely change this and make it possible to predict who develops the disease. That could mean a patient gets the opportunity to start therapies that delay symptoms or completely prevent Alzheimer’s.

The researchers, who published their study in Neurobiology of Aging, employed machine learning to develop an algorithm using PET scans of brains to search for the smallest signs of amyloid plaques. When detected in the brain, these proteins are one of the hallmark signs of Alzheimer’s and may start to build up years (or even decades) before the onset of dementia.

The scientists found their formula predicted disease onset with 84 percent accuracy. This innovation could also be a boon for clinical trials, allowing medical researchers to easily identify patients who may be appropriate study subjects for novel therapies developed to prevent further progression of the disease.


Therapy is often seen as a first-world luxury. But AI has the potential to bring psychological counseling to the masses. Already, it has been used for challenging and costly tasks such as counseling Syrian refugees, according to The New Yorker. A number of companies have been working on chatbot products that communicate with users much like a trained professional would, meaning it’s possible for machines to learn one of the most fundamental qualities of humanity: empathy.

One example is Woebot, a phone app that costs between $6 to $12 a week. The phone app, developed through a randomized controlled trial on stressed-out students at Stanford University, harnesses the power of cognitive behavioral therapy. This approach to counseling helps someone become more aware of—and change—problematic and troublesome behaviors that may alter the person’s mood.

Like a real, live therapist you might pay $100 per hour to visit, this robot shrink will learn more about you over time and become a better counselor as a result. Unlike your therapist, though, this chatbot is there for you 24/7 at the most critical moments, like the middle of the night, when you’re tempted to drunk-text your ex.

Advance Genomic-Based Medicine

Since completing the map of the human genome in 2003, the medical and scientific community has been excited about using the power of Big Data to identify causes and treatments for both common and rare diseases. The problem is that this giant pile of data is, well, giant. But AI is turning genomics into information with real clinical application—what is often called precision medicine.

This approach is already changing cancer care. Machine learning is helping classify tumors by genetic types, allowing doctors to match a patient’s unique disease to the most effective treatments. In June, the American Society of Clinical Oncology announced that the IBM Watson supercomputer was able to generate potential tumor treatment recommendations for 96 percent of patients and reduced the time it takes for screening patients for clinical trials by 78 percent.

Repurpose Old Drugs

Scores of new pharmaceutical drug compounds are developed each year, but very few of them are effective for the diseases and conditions they’re supposed to treat. Some don’t even make to clinical trials, which means many are laid to rest on a shelf in a lab and never picked up again.

AI could help digest data in a way that recognizes disease states and drug pathways and connects them in unexpected ways. This task is typically too arduous for humans to do alone. Bioinformatics is able to expedite this process, meaning old drugs get a new lease on life (and could save lives in the process).