The Union government has approved a 30% cap on trade margins for non-scheduled cancer medicines, seeking to curb the mark-ups that inflate patients’ pharmacy bills. The Department of Pharmaceuticals estimates that the measure could reduce the maximum retail prices (MRPs) of affected drugs by up to 70% and save patients 2,500 crore rupees annually.

The cap will apply to branded and generic medicines, whether manufactured in India or imported, and whether patented or non-patented. An expert committee under the Directorate General of Health Services (DGHS) will identify the medicines covered. The National Pharmaceutical Pricing Authority (NPPA) will then issue the implementation notification.

The government’s estimates are projections. The extent of the price reductions will become clear after the covered medicines and revised prices are notified.

NPPA Finds Mark-ups of Upto 700%

An NPPA analysis found that trade mark-ups on non-scheduled anti-cancer medicines averaged around 170%, with some reaching 700%. Such margins can create a substantial gap between the price at which a medicine enters the distribution chain and the amount charged at the retail counter.

For patients who need costly medicines over multiple treatment cycles, even a modest reduction in the price of each purchase can ease recurring expenses. The effect is particularly relevant to households paying directly for medicines that are not fully covered by insurance or public health schemes.

The 30% limit is intended to restrict the margin added through the relevant stages of distribution and retail. It does not mean that every affected medicine will become 70% cheaper. The reduction will depend on the medicine’s existing price and trade margins.

How India Regulates Medicine Prices

India’s drug-pricing framework distinguishes between scheduled and non-scheduled formulations. The NPPA fixes ceiling prices for scheduled medicines under the Drugs (Prices Control) Order, 2013, with the National List of Essential Medicines (NLEM) forming the basis for coverage.

Non-scheduled medicines generally do not have the same routine ceiling-price controls, although manufacturers are restricted from increasing their maximum retail prices by more than 10% over the preceding 12 months. The government can also intervene in the public interest under Paragraph 19 of the DPCO, 2013.

The new decision uses this intervention power to regulate trade margins across a wider range of non-scheduled cancer medicines. Rather than setting a single ceiling price for every drug in the category, it seeks to limit the margin added as medicines pass through the supply chain.

A precedent from 2019

In February 2019, the NPPA imposed a 30% trade-margin cap on 42 selected non-scheduled anti-cancer medicines. The intervention covered 526 brands and was estimated to save patients 984 crore rupees annually. The authority reported that the maximum retail prices of some brands fell by as much as 90%.

That exercise provides a precedent for using trade-margin regulation to lower medicine prices. The latest measure has a broader proposed scope, although its eventual reach will depend on the list finalised by the expert committee.

The earlier figures should not be treated as a forecast for the new intervention. The medicines covered, their existing margins and the price changes required will determine the savings achieved this time.

Production Must be Maintained

The government has said manufacturers will be required to maintain current production levels. The condition addresses a practical concern in price regulation: patients must continue to have access to prescribed medicines after the pricing rules change.

Implementation will require monitoring both prices and availability. A lower listed price offers little relief if a medicine becomes difficult to obtain or patients must turn to a more expensive alternative.

The DGHS expert committee must identify the medicines covered before the NPPA issues its implementation notification. Until then, patients and pharmacists cannot determine the precise price changes for individual products.

The projected 2,500-crore rupees annual saving will depend on the final list, the reductions achieved and how consistently the revised prices are reflected in sales. The cap addresses the retail cost of medicines; hospital charges, surgery, radiation, diagnostic tests and other treatment expenses fall outside this measure.

For patients managing cancer treatment over months or years, the relevant figure will be the revised price of each prescribed medicine, not the maximum reduction projected for the category as a whole.

More than half a million people are diagnosed with pancreatic cancer around the world each year. For many, the disease is discovered only after it has moved beyond the pancreas. The timing can make a profound difference. In the latest global estimates from the International Agency for Research on Cancer (IARC), more than 530,000 people developed pancreatic cancer in 2024, while more than 490,000 died from it. Although pancreatic cancer is only the 12th most commonly diagnosed cancer worldwide, it ranks sixth as a cause of cancer death.

It is also largely a disease of older adults. In the US, where detailed cancer surveillance data are available, the median age at diagnosis is 71. About two-thirds of patients are at least 65, according to the American Cancer Society.

But age is only part of the problem. Pancreatic cancer can remain difficult to recognise because early disease often causes no obvious symptoms. The pancreas sits deep inside the abdomen, making early tumours difficult to detect through a routine physical examination. When symptoms such as jaundice, weight loss, abdominal or back pain appear, the cancer may already have grown substantially or spread.

That is why researchers are beginning to pursue an idea that changes where the fight against pancreatic cancer starts. Instead of waiting for a tumour to become invasive, they want to identify the abnormal changes that come before it — and stop the disease there. The strategy is called cancer interception.

Why Catching It Early Matters

The numbers show why researchers are looking further upstream. In the latest US SEER data, only about 15% of pancreatic cancer cases are diagnosed while the cancer is still confined to the pancreas. For these patients, the five-year relative survival rate is 43.6%.

Once the cancer has spread to nearby lymph nodes, five-year survival falls to 17%. For patients whose cancer has already metastasised to distant parts of the body, it is just 3.4%. Overall, the five-year relative survival rate is 13.7%. Those figures are not simply statistics about treatment. They explain the urgency behind early detection. If doctors can find pancreatic cancer before it spreads, patients have a substantially better chance of surviving it.

The difficulty is that there is currently no routine screening test recommended for people at average risk. The American Cancer Society notes that no screening test has yet been shown to reduce deaths from pancreatic cancer in the general population. Surveillance is instead considered for people at particularly high risk, such as those with certain inherited genetic risks or strong family histories. So researchers are looking for people who can be watched closely before cancer appears.

Following People Before Cancer Arrives

One of the largest efforts is PRECEDE, a clinical study led by Diane Simeone, director of the Moores Cancer Center at the University of California San Diego Health. The study aims to follow 20,000 people at increased risk of pancreatic cancer. Participants include people with a family history of the disease, certain abnormalities in the pancreas and genetic factors that raise their risk.

More than 12,000 people had enrolled by the time researchers presented an update at the American Association for Cancer Research conference on pancreatic cancer in September. More than 50 pancreatic cancers had been detected among participants, many at early stages.

That makes the study more than an exercise in surveillance. It is creating a group of people who can be followed closely as their pancreatic tissue changes, potentially allowing researchers to see what happens in the period between an abnormality and full-blown cancer.

The researchers are also collecting biological samples to study experimental blood tests that could detect pancreatic cancer earlier. And there is another tool they hope can help: artificial intelligence. Researchers are examining whether AI can identify subtle abnormalities in pancreatic scans before they become apparent to the human eye.

If these approaches work, the goal would be to move diagnosis forward, from the point at which cancer is already established to a much earlier stage in its development. But early detection creates a new question. If doctors find something that could become cancer, can they stop it?

Can the Drug Work Earlier?

A new targeted drug has given scientists another reason to investigate. In August, the US Food and Drug Administration approved daraxonrasib for certain patients with advanced pancreatic cancer. The drug targets KRAS, a protein involved in signals that can drive cancer growth.

In a randomized clinical trial involving 500 patients with advanced pancreatic cancer, median overall survival was 13.2 months for patients receiving daraxonrasib, compared with 6.7 months for those receiving standard chemotherapy.
But the drug’s approval does not mean it can prevent pancreatic cancer.

It is approved for advanced disease. Researchers are interested in what might happen if drugs that target cancer-driving pathways are used much earlier, perhaps when abnormal pancreatic cells have not yet developed into an invasive tumour. That is the central idea behind interception.

Stopping Cancer Early

Treating someone who already has metastatic cancer and treating someone who has a precancerous pancreatic abnormality are completely different medical decisions. For a patient with advanced cancer, the potential benefits of a powerful treatment may justify significant side effects. For someone who has an abnormality that might never become cancer, the calculation is different.

Researchers therefore need to know which precancerous changes are dangerous enough to treat and whether the treatment itself causes more harm than the disease it is intended to prevent. That is why much of the evidence for pancreatic cancer interception is still coming from laboratory and animal studies.

A clue From Mice

At the September AACR meeting, Ben Stanger, a cancer researcher at the University of Pennsylvania, and his colleagues presented research involving mice carrying mutations in the Kras gene. KRAS mutations can activate proteins that promote cancer development. The researchers waited until the mice developed tiny precancerous growths in the pancreas. They then treated the animals with a drug designed to interfere with KRAS and related cancer-promoting proteins.

The treatment improved survival in the mice. The finding matters because it suggests that cancer-driving pathways may be vulnerable even before a pancreatic tumour becomes invasive. The researchers still need to establish whether the same strategy is safe and effective in humans, which patients should receive it, and how early treatment should begin.

From Treating Cancer to Stopping Its Progression

This is what makes cancer interception such a significant shift in pancreatic cancer research. The traditional approach begins after a tumour has formed. Doctors then try to remove it, shrink it or keep it from spreading. Interception moves the starting line. Researchers want to identify the biological changes that put pancreatic cells on the path toward cancer and intervene before that process becomes difficult to reverse.

Simeone’s team is already considering whether therapies such as daraxonrasib could eventually be studied in people after surgery for precancerous pancreatic growths or in patients with very early-stage disease. Such use would require clinical trials; the drug is currently approved for advanced pancreatic cancer. Simeone has estimated that combining earlier detection with interception could potentially raise five-year survival from 13.7% to 50%.

That figure is a research projection, not a demonstrated result.The immediate challenge is much more basic: scientists need to prove that they can reliably identify dangerous pancreatic changes early enough, and that treating them will actually prevent cancer from progressing.

For a disease in which only about 15% of cases in current US data are found while still localized, even finding that window would change the problem researchers are trying to solve. The hope behind cancer interception is therefore not simply to find a better drug for pancreatic cancer. It is to change the moment at which doctors have to fight it, from after it has spread to before it has a chance to become invasive.

The human brain looks like one organ. Its history may tell a different story. A Stanford Medicine study has found that the front and back of the developing brain arise from two separate populations of brain cells, following different developmental paths from the earliest stages of embryonic development.

The finding challenges a long-standing idea that the entire brain grows from a common pool of progenitor cells. It may also solve a problem that has frustrated researchers for years: why some of the neurons that keep us breathing and swallowing have been so difficult to grow in the laboratory. The study was published in Nature Neuroscience on September 18.

Two paths, One Brain

Long before a brain takes shape, its cells begin making choices about what they will become. The Stanford researchers found that one group of early cells, carrying the Otx2 gene, develops into the forebrain and midbrain. A different group, marked by Gbx2, develops into the hindbrain. The two groups do not merge.

They also carry different arrangements of chromatin, the material that packages DNA. Those differences help keep the cells on separate developmental tracks. The hindbrain is not a minor part of the brain. It contains the brain stem and controls functions that keep the body running without conscious effort — breathing, heartbeat, swallowing and other basic processes.

Its neurons are also involved in moving the muscles of the face, tongue and throat. Yet scientists have struggled to make these cells from human stem cells. The new study suggests they may have been starting from the wrong place.

“People are always focused on creating the final cell type, like the neuron,” said Rayyan Jokhai, a graduate student and co-first author of the study. “But it’s important to begin at the earliest stages of embryonic development.”

Brain Cells: From Stem Cells to Working Neurons

The researchers used what they learned about early development to guide human pluripotent stem cells toward a hindbrain fate. It worked. The resulting neurons produced electrical signals and carried molecular markers associated with hindbrain regions involved in facial movement and swallowing.

For researchers studying brain-stem diseases, having these cells in the laboratory could be valuable. In spinal muscular atrophy, motor neurons progressively deteriorate. ALS can damage motor neurons in both the forebrain and hindbrain. As the disease progresses, patients can lose the ability to swallow and, eventually, breathe.

Scientists cannot simply take brain-stem tissue from living patients and watch these neurons deteriorate. Lab-grown human hindbrain neurons could provide another option: researchers can study the cells, investigate what goes wrong and test possible treatments.

An Ancient Split

The story gets older when the researchers look beyond humans. They found the same two-origin pattern in chickens and zebrafish. They also found it in acorn worms, distant relatives of humans.

The pattern appears to reach back more than 550 million years. That suggests the separation is not a recent feature of the human brain. Instead, it may be a very old arrangement inherited from ancestors that lived hundreds of millions of years ago. The researchers propose that evolution brought two ancient neural systems together, eventually producing the integrated brain seen in vertebrates. In other words, what looks like one organ may have a much more complicated family history.

More than a story about brain evolution The finding could reshape how scientists make specialised brain cells in the laboratory. It may also open another line of research. The hindbrain contains neural circuits involved in hunger and appetite, raising questions about its role in metabolic disorders and treatments such as semaglutide.

For now, the Stanford team wants to trace the developmental origins of the spinal cord and understand how diseases such as SMA and ALS damage hindbrain neurons. The cells that eventually become parts of the human brain appear to make fundamentally different choices before there is anything recognisable as a brain. By the time the brain looks like one organ, its cells may already be carrying the history of two very different beginnings.