Paralysis on one side of the body is common after stroke. A new study in CNS Neuroscience & Therapeutics demonstrates that acupuncture can significantly improve muscle function recovery in patients who experienced a stroke, with this recovery correlating to increases in grey matter volume in certain regions of the brain related to cognitive-motor integration.
For the study, 56 patients with stroke were randomly allocated in a 2:1 ratio to receive either true-acupoint or sham-acupoint acupuncture over a 2-week period. Only the true-acupoint group showed significant improvements in motor recovery tests. Increases in grey matter volume in the right opercular inferior frontal gyrus, postcentral gyrus, and cerebellar region of the brain were positively correlated with limb motor function recovery in the true-acupoint group.
“These [brain] modulations may improve motor initiation, execution, control, and coordination, representing a potential central mechanism underlying acupuncture’s therapeutic effect,” the authors wrote.
The long-acting HIV prevention injection, lenacapavir, will become available to around half a million people in South Africa. Photo by Anna Shvets
By Marcus Low and Elri Voigt
On June 5, 2026, an HIV prevention injection will for the first time become available at some of South Africa’s public sector clinics. In this Spotlight special briefing, we pull together all you need to know about this “breakthrough” jab.
We’ve come a long way from the worst days of South Africa’s HIV epidemic, but the virus still claims over 50 000 lives per year and, even in 2026, annual new infections remain stubbornly high at over 140 000.
Reducing the rate of new infections is not an easy task. The most effective measure is to make as many as possible of the roughly eight million people who are living with the disease non-infectious. The good news is that most people with HIV become non-infectious once they are stable on antiretroviral treatment. The bad news is that the growth of South Africa’s HIV treatment programme has slowed. The pool of infectious people thus seems set to remain relatively large.
For people who are not living with HIV, the most effective form of protection over the years have been the correct use of condoms. Condoms also have the benefit that they protect against other sexually transmitted infections.
But condoms aren’t the only game in town. Voluntary medical male circumcision substantially decreases men’s risk of contracting HIV, something that also provides indirect protection for women.
And then there are antiretrovirals (ARVs) taken to prevent HIV infection. Landmark studies published in the 2010s showed that taking a tablet that contains the antiretroviral medicines tenofovir and emtricitabine could reduce someone’s risk of contracting HIV to near zero. Such tablets are commonly referred to as oral pre-exposure prophylaxis, or oral PrEP. For several years now, these HIV prevention tablets have been widely available in South Africa’s public healthcare system, although uptake has been somewhat muted. Modelling work from Thembisa, the country’s leading mathematical model on HIV and TB, suggests that only a few hundred thousand people are taking the tablets.
The long-acting revolution
One challenge with HIV prevention pills is that not everyone can, or wants to, take them every day. For some, taking ARVs, or being seen to take ARVs, still comes with an accompanying dose of stigma. For others, remembering to take a pill every day can be tricky. Ultimately, the incentives for healthy people without HIV to take prevention medicines simply aren’t as compelling and immediate as they are for people who already have the virus in their bodies.
As in some other areas of medicine, one solution to this treatment adherence challenge is simply to make it more convenient to take the treatment. Many women, for example, prefer three-monthly contraceptive injections or three-yearly implants to a regular pill. There is some evidence that similar preferences apply to HIV prevention medicines.
So-called long-acting therapies does what the name suggests – act over longer than standard periods. They could take many forms, from slow-release tablets to injections that leave a depot under the skin that slowly releases drugs into the blood stream, to small implantable devices that are typically left in the arm for several years.
The first long-acting HIV prevention option to take the world by storm was an injection. It made headlines in 2020 when a pivotal study found it to be more effective than the daily prevention pills – the difference being largely due to better adherence, rather than differences in the ARVs used. This jab, containing the antiretroviral drug cabotegravir, provides two months of protection against HIV infection at a time.
Two years later, the World Health Organization recommended the jab, called CAB-LA, for HIV prevention, and it was registered for use in South Africa. Rollout beyond an implementation science setting stalled however when the prices the drug’s manufacturer ViiV Healthcare was willing to sell it for were deemed unaffordable by the South African government.
Fortunately, a new prevention jab that provides protection for three times as long as CAB-LA was on the way. In 2024, two large studies, found an injection of the antiretroviral drug lenacapavir given every six months was almost 100% effective in preventing HIV infection. These findings would later be hailed as the journal Science’s 2024 scientific breakthrough of the year. It is this “breakthrough” that is being rolled out in South Africa from June 2026.
Two often-neglected groups in HIV research, adolescents (aged 16 and 17), and women who become pregnant while in a study, were included in clinical trials of lenacapavir. The jab was found to be safe in both populations, which means it can now be offered to adolescents and pregnant women in the South African rollout.
Lenacapavir is injected just under the skin, typically in the stomach area, where it forms a small depot that very slowly releases the drug over time. These depots can form small lumps under the skin. Though harmless and usually not visible, it will be important that people getting the jab know to expect these “subcutaneous nodules”. The other most common side effects seen in the two pivotal studies were pain at the injection site and a skin rash. These reactions and the size of the nodules appear to decrease with subsequent injections.
Prior to their first injection, people will first have to get an HIV test to ensure they aren’t already living with HIV. This is important since treating someone with HIV with just lenacapavir could result in the development of drug resistance. Together with the injection, people starting lenacapavir will also have to take some lenacapavir tablets for two days. Since the depot releases the injected drug very slowly, these tablets are needed to get the drug levels in the body up more quickly so that it can provide full protection as soon as possible. (The Department of Health has published a guideline document setting out how it should all work at the clinic.)
In addition to the lenacapavir and CAB-LA jabs, there is also a long-acting vaginal ring that contains the ARV dapivirine. The ring provides one-month of protection at a time, with a three-month version also under development. The available evidence however suggests that the dapivirine vaginal ring is not as effective at preventing HIV infection as oral PrEP or the two injectable options.
The long road to jabs at clinics
Having the scientific evidence that an injection works is of course only one step in that jab’s long journey to the point where people can get it at clinics. An essential next step was regulatory approval, which lenacapavir received from the South African Health Products Regulatory Authority in October 2025. After regulatory approval was secured, the next question became whether a sufficient supply of the product can be procured in South Africa on acceptable terms.
Lenacapavir is currently only being produced and marketed by the pharmaceutical company Gilead Sciences, who holds the critical patents on the product. In the US, lenacapavir is sold for around $28 000 per person per year. The Global Fund (the world’s largest multilateral funder of health in low- and middle-income countries) and PEPFAR (the United States President’s Emergency Plan for AIDS Relief) are however procuring limited stocks of lenacapavir at a lower price for use in some low- and middle-income countries. It is some of these Global Fund-procured jabs that will be used in the first phases of the lenacapavir rollout in South Africa.
For now, largely due to the limited stocks, the local rollout will target only around half a million people at 360 clinics in areas with high HIV rates, but the plan is to scale-up considerably in the next few years.
The South African government will likely start buying lenacapavir from generic manufacturers in 2027 or 2028. Gilead has so far issued licenses that will allow six different companies to produce lenacapavir and to sell it in 120 different countries, including South Africa.
The Gates Foundation and a partnership including UNITAID, the Clinton Health Access Initiative, and Wits RHI, have concluded separate deals with generic manufacturers that should see these generics sold for a price of no more than $40 (under R800) per person per year. This is lower than what government currently pays for oral PrEP and modelling work suggests it would be affordable for the South African government. Barring any unforeseen hiccups, the pieces are thus in place to facilitate widespread access to lenacapavir in South Africa in the coming years.
For now, none of the generic versions of lenacapavir will be produced in South Africa. Negotiations are however under way that may eventually see a local company licensed to produce the jab. Such local production is seen as important for ensuring security of supply, although it is not clear that local companies will be able to compete with Indian generic drug-makers on price.
At the time of writing, neither the lenacapavir or CAB-LA injections can be purchased at private sector pharmacies in South Africa. Oral PrEP can be purchased for around R300 for a month’s supply. The monthly dapivirine vaginal ring should cost in the region of R500 per ring. (These prices are based on the 30 April 2026 Single Exit Price database published by the health department.)
How many people will want the jabs?
One of the big unanswered questions about lenacapavir is how many people will come forward to get the jabs. We are hopeful that the Department of Health will routinely provide detailed numbers on uptake in the coming months and years.
The initial rollout is largely clinic-based, but researchers will also be assessing how well distribution works through mobile clinics. We need not stop there of course. At the height of the COVID-19 pandemic, public sector users could access SARS-CoV-2 vaccines from nurses at private sector pharmacies. With sufficient political will, the same could be done with lenacapavir. No doubt some young people will rather get their jab at the mall than at the clinic.
Those in control of the rollout will have to think carefully about how they promote and provide the jab. At its core, it is an empowering tool that can help people stay HIV-free, but as often is the case with HIV-linked products, there is a risk of stigma. In addition, even though lenacapavir is not a vaccine, some vaccine scepticism might well transfer over to lenacapavir since it is administered as an injection. As with any large healthcare intervention, one will not have to look far to find lenacapavir-related misinformation on social media.
Either way, just having the jab at clinics and hoping people will come get it might not be good enough if we’re hoping to see good uptake. Fortunately, we have several research groups and NGOs in South Africa who have world-class expertise on just this type of issue. Hopefully government will draw on this unique reservoir as they adjust and shape the lenacapavir rollout.
So what’s next
The rollout of the lenacapavir jab in South Africa will not be the end of our HIV prevention story. Two promising products in the pipeline are a new formulation of lenacapavir that looks like it could provide a full year of protection per shot and a pill containing another antiretroviral that could provide a month of protection at a time. We are keeping a close eye on the ongoing development of these products. There are also still hopes that an effective HIV cure or vaccine might one day be developed, although this is a much longer shot than better long-acting antiretroviral formulations.
In the meantime, though, twice-yearly lenacapavir is rightly dominating the headlines.
Modelling suggests that over the next 20 years, an ambitious lenacapavir rollout could reduce new HIV infections by around 20% to 30%. There can be little doubt that, like condoms and antiretroviral treatment for people living with HIV, providing lenacapavir at scale makes public health sense.
But thinking of lenacapavir mainly in terms of cost-effectiveness and public health benefits risks obscuring its more immediate and transformative human potential. For many people, especially young women, a discreet and convenient form of HIV prevention that they can control may well make the difference between contracting HIV or not.
As experts often point out, when it comes to products that can prevent HIV, choice – as in the world of contraception – is key. Some products will work for one person, but not for others. As circumstances change, a product that might have once worked may no longer be the best option. Having more than one product in the “toolkit of prevention” makes it easier to find what actually works in people’s lives.
For years, the HIV world has been flush with rhetoric about empowering young women – a group that is profoundly affected by HIV. An ambitious lenacapavir rollout might be the most concrete realisation of those ideals yet. We simply have to get it right.
Disclosure: The Gates Foundation is mentioned in this article. Spotlight receives funding from the Gates Foundation, but is editorially independent – an independence that the editors guard jealously. Spotlight is a member of the South African Press Council.
Researchers at the Terasaki Institute for Biomedical Innovation and University of Arizona College of Medicine, have developed a topical gel formulation with 4-aminopyridine (4-AP) to treat burn wounds, achieving near-complete closure in 21 days. The findings are published in the journal Biomaterials.
Burn injuries rank among the most difficult wounds to heal. The current gold standard, transplanting skin from a donor site on the patient’s own body, is limited by donor site morbidity and the need for large amounts of healthy tissue. This research offers a non-invasive alternative: a laponite-gelatin gel that delivers 4-AP directly to the wound, concentrating the drug where it is needed rather than exposing the whole body to it. Prolonged systemic use of 4-AP can cause serious side effects, including seizures, making localised delivery a critical advance.
The drug is best known under the brand name Ampyra for treating multiple sclerosis. Earlier work showed it could influence keratinocytes and fibroblasts: the two cell types central to skin repair, but systemic administration carried unacceptable risks. Embedding it in a gel resolves that problem while preserving its therapeutic potential.
“By delivering 4-AP directly to the wound site, we harness its regenerative potential while avoiding the systemic risks that have limited its use. We believe this approach could meaningfully change how burn injuries are managed clinically,” said Dr. Johnson V. John, Assistant Professor at the Terasaki Institute for Biomedical Innovation
Laboratory tests confirmed that the gel releases 4-AP at a controlled rate, is compatible with living cells, and produces more than 90% wound closure within 48 hours. In animal studies, treated wounds closed faster than controls starting at day six, reaching near-complete closure by day 21, while control wounds remained partially open. Tissue analysis showed the gel reduced inflammation, promoted re-epithelialisation and angiogenesis, and drove fibroblast-to-myofibroblast transformation. Collagen deposition increased markedly by 438% for type I and 288 percent for type III versus controls (P < 0.05 to P < 0.0002), with an improved collagen ratio signalling better-quality tissue maturation.
Because 4-AP is already FDA-approved with a well-characterised safety profile, this repurposing strategy could accelerate the path to clinical trials compared with developing an entirely new compound from scratch.
“This research exemplifies our commitment to reimagining existing therapies to address medicine’s most persistent challenges. We look forward to seeing it advance toward clinical application,” stated Xiling Shen, Acting Director of the Terasaki Institute for Biomedical Innovation.
Drug-resistant Salmonella. Credit: CDC on Unsplash
Researchers at McMaster University have discovered a new antibiotic that kills some of the world’s most dangerous and drug-resistant bacteria – and does so by targeting a previously unknown vulnerability, opening the door to an entirely new class of treatments.
The new compound, called manikomycin, was identified by a team led by McMaster Professor Gerry Wright and has shown early effectiveness against priority pathogens including Salmonella, E. coli and Klebsiella.
Unlike any antibiotic currently used in clinics, it works by blocking the exit site of the ribosome, the protein-producing machinery found inside every bacterial cell.
The discovery, published today in Nature, marks the fourth new antibiotic candidate from Wright’s lab in just over a year, underscoring a promising new approach to drug discovery at a time when antibiotic resistance is a growing global threat.
“So we’ve not only found a brand-new drug candidate, but we’ve also established a brand-new target in bacteria that could potentially be exploited with other new drugs.”
It’s the latter part of the discovery that has researchers most excited. Wright notes that because most antibiotics in use today target the same handful of vulnerabilities on the ribosome, bacteria have evolved broad defence strategies against such attacks. However, drugs that attack a different part of the ribosome – the exit site – leave them defenceless.
“Even newly discovered drugs that attack those same old targets may quickly face resistance,” says Wright, a professor in McMaster’s Department of Biochemistry and Biomedical Sciences.
“But across the history of medicine, we’ve put absolutely no selective pressure on this particular target, so bacteria have no existing resistance mechanisms for manikomycin.”
Wright likens the ribosome to a factory assembly line. Finished components, he says, must be moved off the line before the next piece can advance. Manikomycin blocks the exit lane, causing the entire assembly process to jam and eventually grind to a halt. And, without the ability to produce proteins, bacteria cannot survive.
The discovery of manikomycin builds on work that began more than 75 years ago, when scientists first discovered that the soil bacterium Streptomyces rimosus produced oxytetracycline, a powerful new drug that would help usher medicine into the antibiotic age.
While the breakthrough was one of several like discoveries made in the mid-1900s, S. rimosus and related bacteria have long since been abandoned as a potential source of new antibiotics.
“There is an overwhelming perception in science that these bacteria have been mined completely dry – that we’ve found all there is to find,” Wright says. “Our lab has found that this is not at all the case.”
Wright’s group, working with collaborators at the University of Illinois Chicago and the University of Hamburg in Germany, used an advanced laboratory technique called fractionation to uncover the new antibiotic.
By filtering out oxytetracycline and other abundant compounds from the chemical mixtures produced by S. rimosus, the researchers were able to isolate scarcer molecules that had gone unnoticed over the years.
Manpreet Kaur, a postdoctoral fellow in Wright’s lab and first author on the new study, says that finding a viable new drug candidate this way signals new opportunities for antibiotic discovery.
“There is likely so much still to be discovered through fractionation,” says Kaur. “Revisiting the extracts of even-well studied bacteria like Streptomyces may lead to similar discoveries in the future.”
Wright’s team is now advancing manikomycin toward clinical development. They have already shown that the new antibiotic is not toxic to human cells, and that it works well in a lab-controlled model of infection – both key milestones on the early development pathway.
They are now working on optimiaing the drug’s “residency time” – or how long it stays active in the body – and have produced 60 derivatives, with plans to push the best one forward.
“We’re excited about this molecule’s potential,” Wright says. “There’s a clear path forward, and we may even be able to expand its spectrum so that it eventually affects even more bacteria, too.”
Haematuria, the presence of blood cells in urine, is a sign of bladder cancer. Because aspirin blocks platelets from forming harmful blood clots, the medication can cause mild bleeding or worsen existing bleeding in the urinary tract. Results from a study in the Journal of Internal Medicine suggest that this may prompt a clinician to run tests that uncover an asymptomatic bladder tumour.
For the study, investigators analysed information on 50 771 Danish adults who started taking aspirin in 2005–2023, as well as 156 191 who started non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs), which have less pronounced antiplatelet abilities than aspirin.
Compared with adults from the general population who have never used aspirin or NSAIDs, aspirin initiators received more cystoscopies – minimally invasive procedures that allow a doctor to view the inside of the bladder and urethra with a lighted tube equipped with a camera. Cytoscopy results showed that recent aspirin initiators had a similar bladder cancer prevalence, but a lower prevalence of invasive stage compared with never-users. This suggests that individuals initiating aspirin treatment represent a patient population with a higher incidence of bladder cancer, and that their higher cystoscopy rate reflects this and thus is clinically warranted. The combination of a larger proportion of relevant cystoscopies and a lower prevalence of invasive cancer stage at diagnosis may represent unmasking of otherwise asymptomatic bladder cancer.
NSAID initiators received more cystoscopies than never-users, but they had a lower bladder cancer prevalence after cystoscopy and a similar stage distribution as never-users. This suggests that the higher cystoscopy rate may not have been clinically warranted.
“We are very encouraged by these results. In the clinical setting, they underline the importance of acting on suspicious bladder cancer symptoms among aspirin initiators,” said lead author Malene Söth Hansen, MD, of Aarhus University. “The findings may further have implications for the question of whether aspirin can prevent bladder cancer, as detection in trials with short-term follow-up may appear as a higher incidence in the aspirin-exposed cohort.”
Bans on teenagers’ social media use are gathering pace worldwide. Their proponents claim that social media bans will improve young people’s mental health, but what evidence supports these claims? In their new Frontiers in Developmental Psychology article, Dr Monika Neff Lind and her co-authors argue that there is no solid scientific evidence behind these bans, and reason to believe they could backfire. In this guest editorial, Neff Lind explains why she and her colleagues doubt that social media bans will work, and how bans should be evaluated to determine whether they have any positive effects.
By Monika Neff Lind, PhD
In December 2025, Australia banned young people under 16 from having social media accounts. France, Greece, Spain, Denmark, Malaysia, Norway, India, Egypt, Canada, Türkiye, and the United Kingdom are hot on their heels. French president Emmanuel Macron said, “Banning social media for those under 15: this is what scientists recommend.” American senator Brian Schatz, author of the Kids Off Social Media Act, said, “Studies have revealed that when children and teens reduce or eliminate exposure to social media for longer than a month, their mental health benefits.” Proponents of youth social media bans claim that we have strong scientific evidence showing that bans will improve teenagers’ wellbeing.
As a clinical psychologist and parent, I would be thrilled if this were true, but it is not. We do not know how social media bans will affect youth because we have never studied that question. Let me explain.
Searching for evidence
When we want to test claims like ‘banning social media improves youth wellbeing’, scientific experiments are one of our most powerful tools to figure out what is causing something to happen. In experiments testing the effects of social media restriction on wellbeing, we randomly assign people to at least two groups: one quits using social media for a period of time and the other is the control or comparison group, which continues to use social media as usual. Given the strength of ban proponents’ claims, my co-authors and I were curious to know how strong the experimental evidence supporting their position was. In our new study, we collected and reviewed all of the experiments that have tested whether social media restriction improves wellbeing, and we were shocked by what we found.
Not a single social media restriction experiment has included people under the age of 16. We do not know how social media bans will affect the young people being targeted by them because we have never tested this with them!
To be fair, sometimes strong evidence in adults warrants making the leap to apply the same conclusions to teenagers. But even that leap is not justified here. The experiments with adults show weak, null, and mixed effects, with 40% of experimental studies showing harmful effects (eg, decreased life satisfaction and increased loneliness) or no effects of social media restriction. So even when adults are told repeatedly that social media is bad for their mental health and that giving it up will help, we find, on average, few to no benefits.
There is also good reason to believe that bans may backfire. First, enforcing a youth social media ban raises major ethical concerns. Enforcement efforts invade people’s privacy and are likely to hurt marginalized people more. For example, the technology that determines age based on selfie uploads makes more mistakes with young faces and people of color. Banned youth may also miss out on important resources and communications provided via social media, as schools, clubs, and most other youth-serving organizations use social media as a main form of communication.
What happens when enforcement efforts fail? Many young people will circumvent bans by creating fraudulent ‘adult’ accounts or lurking anonymously. They will retain access to social media without any of the benefits of parental controls or content filters enabled by youth accounts. The vast majority of young people oppose youth social media bans, and teens are well known for their defiance of top-down edicts that disregard their needs. Expect more conflict between teens and caregivers, not less.
To recap, we don’t know how social media bans will affect teens, and the bans may backfire. Yet the bans are still happening! Like other policies that consume resources, political capital, and time, it is imperative for governments to evaluate these actions by funding comprehensive assessments of the bans’ impacts.
What next?
The first step in measuring the impact of these bans is to determine if the bans actually change teenagers’ social media habits. Three months in, Australian authorities reported that close to 70% of social media accounts owned by people under 16 remained active.
Second, we need a careful and well-resourced plan to measure both positive well-being and mental health problems from multiple sources, including self-report, caregiver report, and objective behavioral data, to get a full picture of whether and how altered social media use affects youth.
Third, we need creative approaches to capture the real-world impacts of the bans, since true experiments are not possible and effects may be at the community as well as the individual level. For example, we could randomly assign a subset of youth (eg within a certain region) to delayed enactment of the ban. Whatever approach is taken, governments must collaborate with diverse stakeholders – including young people – to rigorously and openly evaluate potential impacts. Rushed or improvised assessment will leave room for politicization and motivated reasoning.
Big Tech has become infamous for ‘moving fast and breaking things’. Policymakers rushing to enact these bans risk repeating Big Tech’s mistakes and compounding the problems the bans are trying to solve. We cannot ban our way out of a youth mental health crisis. Rather than take things away, we should make things better.
About the author
Dr Monika Neff Lind is a clinical psychologist, science communicator, and researcher in digital mental health based at the University of California Irvine. See more of her work here.
A model using 71 proteins associated with retinal degradation could predict risk in diabetics
Plasma proteomic signatures for early risk stratification of diabetic retinal neurodegeneration. Credit: Wei Wang and Huangdong Li / Zhongshan Ophthalmic Center, Sun Yat-sen University (CC-BY 4.0, https://creativecommons.org/licenses/by/4.0/)
An AI-assisted model based on 71 different blood proteins could help doctors better predict retinal degeneration in diabetic patients before symptoms occur, according to a study published June 2nd in the open access journalPLOS Medicineby Huangdong Li from the Guangdong Provincial Clinical Research Center for Ocular Diseases in Guangzhou, China, and colleagues.
More than half a billion people around the world are now affected by diabetes. People with the disease are at risk of different neurodegenerative conditions, including the breakdown of the retina, the part of the eye that detects light, in a condition called diabetic retinal neurodegeneration (DRN). It can cause severe visual impairment and vision loss, and scientists believe that DRN is a “window” into the diabetic degeneration of other parts of the nervous system, including cognitive impairment and dementia, as well as degradation of nerves in peripheral areas like the fingers and toes.
Unfortunately, DRN is only detected after symptoms appear, when damage is already irreversible. To better predict who might suffer from DRN and when, the researchers sampled the blood plasma from 1492 patients in the Guangzhou Diabetic Eye Study with type 2 diabetes who did not yet have DRN, and examined the eyes of 1218 of them through scans over a six-year period. They compared their results with another 502 people with diabetes in the United Kingdom BioBank.
The researchers identified 71 different plasma proteins associated with DRN. The proteins were part of cell pathways for processes like inflammation and cellular maintenance. Using machine learning, the scientists used the protein levels in plasma to develop a predictive model called Pro-DRN which was able to improve on the best-performing model by 26 percent. The scientists have already put the model online to allow doctors to assess the risk. While Pro-DRN is based on plasma protein levels and relies on associations between protein levels and DRN and not direct causes, the authors hope that it could help doctors predict and potentially prevent neurodegeneration, using a simple blood test analysed by AI.
The authors add, “Our study suggests that early retinal nerve damage in diabetes leaves measurable signals in the blood. By combining plasma proteomics, longitudinal retinal imaging, and explainable AI, Pro-DRN may help move diabetic eye care from detecting established damage toward earlier, molecularly informed risk stratification, so that closer monitoring and future neuroprotective interventions can be directed to the people most likely to benefit.”
The South African National Blood Service (SANBS) and J’Something Bring Blood Donation into the Culture
What if saving a life was part of your weekend plans?
On 6 June 2026, music, culture, community and purpose will come together at Artistry JHB as the South African National Blood Service (SANBS), musician and entrepreneur J’Something host One Day x SANBS Community Blood Drive a unique event designed to make giving blood more accessible, engaging and relevant to a new generation of South Africans.
Every day, blood donors help create more tomorrows for patients across the country. They make it possible for someone to celebrate another birthday, return home to their family, pursue their dreams, or simply get a second chance at life. Yet many South Africans who are eligible to donate have never taken that first step.
Through this purpose-driven partnership, SANBS and J’Something are bringing blood donation into spaces where people naturally connect, create and inspire one another. By blending culture, creativity and community impact, the One Day x SANBS Community BloodDrive aims to show that donating blood is not only life-saving it’s something everyone can be part of.
The result is more than a blood drive. It’s a day party with purpose, where every donation has the potential to save up to three lives.
Secure your spot at the blood drive by completing the quick eligibility screening below.
Whether you’re donating blood or simply coming through to support the movement, expect good music, great energy and a community united for a meaningful cause.
For a long time, the likelihood of surviving pancreatic cancer has been extremely low. For patients who were diagnosed with metastatic pancreatic cancer between 2015 and 2021, about 97% died within five years of their diagnosis.
Pancreatic cancer is so deadly in part because there are no effective screening tests, and it rarely causes noticeable symptoms in its earliest stages. By the time a patient experiences signs, such as jaundice – a yellowing of the skin – or abdominal pain, the cancer has often already spread to other organs.
As a gastrointestinal oncologist and researcher specialising in early-phase clinical trials, I have seen the critical need for more effective therapies for patients with pancreatic cancer. For decades, successfully targeting the central mechanism that causes the vast majority of pancreatic cancers was considered impossible.
However, that narrative is rapidly changing with a new drug that can shut down the key protein that drives pancreatic cancer, nearly doubling survival rates for patients with advanced stages of the disease.
‘Undruggable’ tumours
The standard treatment for advanced pancreatic cancer has historically relied on chemotherapy, potent drugs designed to kill rapidly dividing cells. While chemotherapy can slow the progression of the disease, its effectiveness is often limited by the ability of pancreatic cancer cells to develop resistance against these drugs.
Pancreatic cancer’s success lies in its genetics. More than 90% of pancreatic tumours are driven by mutations in a gene called KRAS. This gene codes for proteins that function as switches that turn cell growth on and off. When the KRAS gene is mutated, the switch becomes permanently stuck in the “on” position, commanding cancer cells to multiply endlessly.
For decades, scientists considered KRAS to be “undruggable.” The surface of the protein is exceptionally smooth, lacking the molecular pockets that standard drugs require to bind to and turn the switch off.
Because existing drugs haven’t been able to target this protein, treatment for pancreatic cancer has primarily relied on toxic drugs that act more like blunt instruments than precise tools. Chemotherapy attempts to control the disease through widespread cell destruction, causing significant collateral damage to healthy tissues that lead to side effects.
Daraxonrasib is taken daily by mouth. Instead of binding to KRAS directly, it attaches to a molecule called cyclophilin A in cells that helps fold proteins into their final 3D structures. This protein complex is then able to bind to the active KRAS protein and shut down its ability to signal cancer cells to multiply.
The company developing the drug, Revolution Medicines, presented results on May 31, 2026, from its Phase 3 clinical trial of 500 patients with metastatic pancreatic cancer who had received prior treatment. Compared to standard chemotherapy, daraxonrasib nearly doubled overall survival from 6.7 months to 13.2 months after diagnosis. Overall, daraxonrasib reduced the risk of death for metastatic pancreatic cancer patients by 60%. https://www.youtube.com/embed/sIspXSWQn1w?wmode=transparent&start=0 Daraxonrasib nearly doubled survival for patients with advanced pancreatic cancer compared to chemotherapy.
The most common side effect is a prominent skin rash, which affected more than 86% of patients in the study. Patients also frequently dealt with stomatitis – painful swelling and sores inside the mouth – as well as diarrhoea, nausea and vomiting. However, patients taking daraxonrasib were far less likely to stop treatment due to severe side effects compared to chemotherapy, and they had improved quality of life with reduced pain.
Next steps for daraxonrasib
By successfully targeting the specific genetic mutation that drives the vast majority of pancreatic cancers, researchers have demonstrated that this “undruggable” disease is treatable with targeted therapy.
The immediate next step is regulatory review of the drug’s readiness for the clinic. With data now officially published, Revolution Medicines will use these findings to seek formal approval from the Food and Drug Administration and other global regulatory bodies.
Because advanced pancreatic cancer is notoriously difficult to treat, breakthrough therapies that demonstrate this kind of significant survival benefit are often granted expedited or priority review. When daroxonrasib becomes available to patients will depend on the review timeline. Should the drug obtain approval, it could be available in clinics within months.
For the broader landscape of drug development, this milestone represents a likely shift in pancreatic cancer treatment. I expect more clinical trials exploring combination therapies pairing KRAS inhibitors with other drugs to prevent tumours from developing resistance to treatment.
Should daraxonrasib succeed, it could help set the stage for more precise, personalised and effective treatments for pancreatic cancer in the years to come.
A new study published in JAMA Network Open found that removing olfactory groove meningioma, a type of brain tumour located near the base of the brain, may improve blood sugar control in patients with diabetes.
Researchers followed patients with an olfactory groove meningioma and diabetes over five years after surgery, tracking long-term changes in haemoglobin A1c (HbA1c), which is a standard measure of blood sugar control, and body weight after tumour removal surgery.
The research team found:
Blood sugar control improved after tumour removal in most patients.
Improvements often happened soon after surgery and lasted for years.
Many patients also lost weight after surgery.
Improvements occurred even when diabetes medications stayed the same.
“This type of brain tumour affects both frontal lobes simultaneously and is usually thought of as causing symptoms like vision problems, personality changes or loss of smell,” said Andrew Venteicher, MD, PhD, an associate professor at the University of Minnesota Medical School and neurosurgeon with M Health Fairview. “What surprised us was how much blood sugar control improved after surgery in many of these patients. The findings may help us better counsel patients before surgery and raise new questions about how the brain influences metabolism throughout the body.”
The findings suggest that some brain tumours may affect the body’s ability to regulate metabolism and blood sugar, and that removing certain brain tumours may improve blood sugar control and weight in some patients with diabetes, in addition to improving neurological symptoms.
Future studies will explore why these metabolic improvements occur and whether similar effects are seen in patients with other types of brain tumours. Researchers also hope to better understand how brain function, behaviour and metabolism are connected and whether these findings could help guide future treatment decisions.
