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241

Oncology

CREATE Medicines Raises $122M for Next-Generation CAR-T Therapies

CREATE Medicines, a biotechnology startup previously known as Myeloid Therapeutics, has secured $122 million in new funding to advance its medical research. Backed by investors including Newpath Partners and ARCH Venture Partners, the company is developing a specialized form of treatment known as CAR-T therapy. This approach typically involves reprogramming a patient's own immune cells to fight disease. However, CREATE Medicines is taking a unique path by utilizing myeloid cells, a specific type of immune agent, to power their therapies. Originally focused primarily on cancer, the company is designing these myeloid cell therapies with the specific goal of attacking solid tumors. This is a major focus in oncology, as solid tumors are often highly resistant to traditional treatments. Recently, CREATE Medicines also expanded its research pipeline to explore how this same technology might be deployed to treat autoimmune diseases. While the science is promising, the research is still in its earliest phases. The recent influx of funding is specifically intended to propel the company's first drug candidates through initial human trials. Because of this early-stage status, clinical safety and effectiveness data have not yet been established, and rigorous testing will be required to see how well these therapies perform in actual patients.

STAT News · 2 min read

242

Drug Development

Biogen's Alzheimer's Drug Clears Toxic Protein but Misses Key Goal

Biogen recently announced results from a mid-stage clinical trial for a new Alzheimer's disease treatment called diranersen, also known as BIIB080. Unlike many well-known treatments that target a substance called amyloid, this new drug targets tau. Tau is a protein that can become toxic to brain cells, known as neurons, and is widely believed to play a major role in the memory loss and cognitive decline associated with Alzheimer's. In the Phase 2 study, the drug successfully reduced the levels of this toxic tau protein in both the brains and spinal fluid of patients with early-stage Alzheimer's disease. Even more encouraging, the company noted that these reductions in tau were linked to a slowing of cognitive decline, suggesting the drug might help preserve memory and thinking skills. However, the trial results were ultimately mixed because the study missed its main statistical goal. Researchers tested three different dosing levels, expecting the highest doses to produce the strongest effects. Instead, the lowest dose actually produced the best results. Because the trial failed to show a traditional dose response, where more medication predictably equals a greater effect, scientists will need to continue investigating how best to use this treatment safely and effectively.

STAT News · 1 min read

243

Drug Development

Biogen advances Alzheimer's tau drug despite missing main trial goal

Biogen and Ionis Pharmaceuticals have been testing a new drug candidate aimed at treating Alzheimer's disease. The experimental medication targets tau, a protein that forms abnormal tangles in the brains of Alzheimer's patients. However, during a phase 2 study, which is a mid-stage clinical trial used to evaluate a drug's effectiveness, the medication missed its primary endpoint, or main predefined goal. Researchers had anticipated seeing a clear dose-response relationship, meaning different amounts of the drug would produce predictably different levels of effectiveness, but the trial failed to generate this data. Despite missing the main objective, the drug did show promising signs elsewhere. Researchers observed reductions in the abnormal tau pathology, and the medication yielded cognitive benefits for the patients. Encouraged by these positive secondary findings, Biogen has committed to moving the candidate forward into registrational development. This means they will conduct the larger, late-stage trials that are required to potentially seek formal regulatory approval for the drug.

Fierce Biotech · 1 min read

244

Drug Development

Repurposed Drug Relieves Psoriasis in Early Mouse Studies

Psoriasis is a chronic condition known for causing itchy, inflamed skin plaques, but it is also closely linked to the body's internal metabolism. In a recent study, researchers identified a specific gene called AKR1B10 that is unusually active in psoriasis. This gene is strongly tied to the presence of activated immune cells that drive the disease. To see if they could interrupt this process, scientists turned to an existing drug called Epalrestat, which is known to block the activity of this specific gene. To test their theory, the research team treated mice that had a psoriasis-like skin condition with Epalrestat. The results were highly encouraging. The drug successfully healed skin lesions and significantly lowered standard scores used to measure psoriasis severity. When looking at safety, Epalrestat actually outperformed methotrexate, a powerful immunosuppressant drug commonly prescribed to patients today. The researchers also uncovered exactly how the treatment works. By inhibiting the AKR1B10 gene, Epalrestat helps restore the natural balance of retinol, also known as vitamin A, in the body. Fixing this metabolic process creates a domino effect that indirectly shuts down IL-17, a major inflammatory signaling pathway responsible for psoriasis symptoms.

PubMed · 1 min read

245

Diagnostics

Whale-Inspired AI Shows Promise for Accurate Cancer Detection

Diagnosing cancer early and accurately is crucial, but it is a complex task. Different types of cancer can look very similar on a medical scan, while cells from the exact same cancer can appear surprisingly different. To tackle this visual puzzle, researchers rely on deep convolutional neural networks, or CNNs. These are advanced artificial intelligence models designed to analyze images. However, getting these models to perform perfectly requires complex, often inefficient, mathematical tuning. To solve this, researchers developed a new system that pairs a standard medical imaging AI, known as VGG-16, with problem-solving algorithms inspired by nature. These "metaheuristic" optimizers automatically adjust the AI's settings to find the most efficient path to an accurate diagnosis. The team tested six different nature-inspired algorithms to see which could best train the AI to recognize complex malignancies. The researchers evaluated their framework on two challenging sets of images: a five-class dataset for cervical cancer and a three-class dataset for lymphoma. The nature-inspired tuning significantly outperformed standard AI models. Remarkably, the Whale Optimization Algorithm, a mathematical model inspired by the hunting behavior of whales, performed the best. It helped the AI achieve up to a 100 percent accuracy rate in classifying the medical images during the testing phase.

PubMed · 2 min read

246

Oncology

How a History of Cancer Impacts Colorectal Cancer Outcomes

Imagine getting diagnosed with colorectal cancer, but it is not your first time battling the disease. Researchers recently looked at a massive national database of over 576,000 patients treated between 2004 and 2022 to understand how having a previous, unrelated cancer affects a person's experience with colorectal cancer. They split the patients into two equal groups, comparing those with a prior history of cancer to those facing a malignancy for the first time. The results revealed a complex picture. Interestingly, patients who had survived a previous cancer were actually less likely to be diagnosed with advanced-stage colorectal cancer or early-onset disease. Their tumors were also less likely to have KRAS mutations, which are specific genetic changes that can cause tumors to grow aggressively. However, the broader outcomes were more concerning. Patients with a prior cancer history faced a 19 percent higher overall risk of death compared to people with no previous cancer, as well as higher mortality rates across most stages of the disease. Researchers noted several factors that might explain these harder journeys. Patients with past cancers often experienced delays in their treatment and were more likely to be readmitted to the hospital after surgery. Their tumors were also more likely to show microsatellite instability, a genetic condition where cancer cells have trouble repairing errors in their DNA. Because this study looked back at past medical records, the researchers emphasize that it only shows correlations, not direct causes, and there may be other unmeasured factors at play.

PubMed · 2 min read

247

Oncology

Precision immunotherapy shows promise for certain childhood brain tumors

Childhood brain tumors are a leading cause of death in kids, and doctors have long hoped that modern immunotherapy could help. One promising type of treatment involves drugs called immune checkpoint inhibitors, which work by taking the molecular brakes off the immune system so it can recognize and attack cancer cells. However, a new comprehensive review of 40 studies reveals that when these drugs are given to children with brain tumors without checking for specific biological markers, the results are largely disappointing. For the vast majority of these patients, tumors shrink in 6 percent or fewer of cases, and the disease typically starts progressing again within one to three months. The challenge is that most pediatric brain tumors are immunologically "cold," meaning they do not naturally attract the immune cells needed to fight the disease. But there is a major exception. The researchers found that checkpoint inhibitors can be highly effective for a specific group of children whose tumors have high numbers of genetic mutations. Patients with "mismatch repair-deficient" or hypermutant tumors experienced long-lasting benefits from the drugs. In this highly specific group, the two-year survival rate was approximately 50 percent. While the treatments do carry risks, the safety profile is generally acceptable, with severe side effects occurring in about 15 to 25 percent of patients. The study authors caution that the current evidence is still in its early stages. The available data is limited by small sample sizes, varying patient populations, and a lack of direct comparison groups in the studies.

PubMed · 2 min read

248

Drug Development

New computer maps reveal hidden weak spots in deadly microbes

Every living cell needs energy to survive. The process that generates this cellular fuel is called glycolysis. Because infectious microbes like Staphylococcus aureus (a dangerous bacterium) and Plasmodium vivax (a parasite that causes malaria) rely heavily on this process, scientists have long wanted to shut it down to cure infections. The problem is that human cells use glycolysis too. Traditional drugs that block the main engine of this energy process often end up harming patients along with the infection. To solve this, researchers used advanced computer models to look for alternative weak points, known as allosteric sites. Think of these as hidden control switches located away from the main active area of the enzyme. By mapping all ten enzymes involved in the glycolysis process for both the bacterium and the malaria parasite, the team found switches that look very different from the ones in human cells. This difference is crucial because it means future drugs could hit these targets to starve the bugs without hurting the human host. Using computer simulations, the team screened over 1,600 existing, FDA-approved drugs to see if any could latch onto these newly mapped hidden switches. They identified compounds capable of binding to multiple targets at once, effectively shutting down the entire microbial energy pathway. However, the scientists caution that this is early work. Because the study relies heavily on computer modeling and virtual screening, researchers will need to test these drugs in physical lab experiments and living models to confirm they work as predicted.

PubMed · 2 min read

249

Oncology

How Pancreatic Tumors Build a Self-Sustaining Network

Pancreatic cancer is notoriously difficult to treat, in part because the tumors build highly complex and protective homes for themselves. New research published in the journal Developmental Cell reveals exactly how these cancer cells cooperate to build a self-sustaining ecosystem. They do this by hijacking a vital biological communication channel known as the Wnt pathway. In healthy biology, Wnt signaling is a set of protein messages that tells cells how to develop and grow. Pancreatic tumors, however, use these same signals to fuel their own relentless expansion. The researchers discovered that this hijacked communication network is far from random. Instead, it is highly organized and varied across the physical space of the tumor, a characteristic scientists call heterogeneous. The cancer cells actively work together to distribute these signals throughout the surrounding tumor microenvironment. Most importantly, the study proves that this cooperative, organized signaling network is absolutely required for the tumor to survive and grow.

PubMed · 1 min read

250

Drug Development

Protein Destroyers Outperform Standard Drugs in Early Cancer Tests

In the search for better cancer treatments, scientists are exploring a clever molecular trick called PROTACs. These are specialized molecules that act like cellular garbage disposal tags. Instead of just blocking a problematic protein from doing its job, which is how traditional drugs called inhibitors work, PROTACs mark the bad protein so the cell's natural waste system completely destroys it. Researchers recently tested this targeted approach on a specific protein called USP7, which plays a complex role in solid tumors. To see how well this trashing method works, the research team created a library of these protein degraders and tested them against traditional inhibitors in melanoma and pancreatic cancer cells. They discovered that the PROTACs successfully and highly specifically targeted the USP7 proteins. Interestingly, getting rid of USP7 changed the mix of other proteins inside the cancer cells, though it did not actually stop the cells from growing in these specific lab tests. The real surprise came when researchers looked at the traditional drugs used to block USP7. They found that leaving these standard inhibitors in the cells for an extended time caused a cascade of unintended metabolic problems. The traditional drugs started affecting other, completely unrelated proteins. This showed that the new protein degraders are far more precise, avoiding the messy off-target effects of the older drugs.

PubMed · 2 min read

251

Oncology

Targeted Immunotherapy Could Fight Cancer With Fewer Side Effects

Immunotherapy is a powerful tool in the fight against cancer. Doctors often use it before surgery, a step known as neoadjuvant therapy, to help shrink solid tumors so they can be successfully removed. While giving these immune-boosting drugs to the whole body works well, it comes with a major catch. Patients frequently experience severe side effects because their entire immune system goes into overdrive, and sometimes the cancer still builds up a resistance to the treatment. Researchers are exploring a more focused alternative. Instead of flooding the entire body with drugs, they are looking at delivering lower doses of immunotherapy directly to the tumor and the nearby lymph nodes, which act as the local filtering system for the body. By keeping the medication localized, doctors hope to spark a much stronger immune response right where it is needed most. This targeted approach could lower the chances of the cancer returning while significantly cutting down on harmful, body-wide side effects. This localized method also gives scientists a unique research advantage. When the tumor is eventually removed during surgery, researchers can examine the tissue closely to see exactly how the immune system reacted and how the cancer might be trying to survive. This hands-on look helps doctors better understand the microscopic battlefield and design better future treatments.

PubMed · 2 min read

252

Oncology

Tracking the immune response to electrical therapy in prostate cancer

Prostate cancer is the second most common cancer in men worldwide. Traditional surgery can be highly effective but often brings life-altering complications, like urinary incontinence and sexual dysfunction. Irreversible electroporation, or IRE, has emerged as a promising alternative. This treatment uses targeted electrical pulses to destroy tumor cells without generating heat, preserving nearby delicate nerves and blood vessels. Scientists have suspected that IRE might also trigger the body's immune system to fight the cancer, but the exact details of how this works in humans have remained unclear. To understand this process, researchers recently tracked the immune systems of five men with localized prostate cancer, analyzing their blood before and one week after IRE treatment. They discovered that the electrical therapy triggers a two-way shift in the immune system. On one hand, the body's rapid-response troops, including natural killer cells and myeloid cells, ramped up. These cells became highly active and ready to destroy targets. At the same time, the chemical chatter between immune cells shifted, becoming more inflammatory but less focused on presenting new tumor markers to the rest of the immune system. Interestingly, the body's precision fighters, called T cells, reacted differently. At the one-week mark, circulating T cells actually dialed back their activation and replication, entering a relatively quiet state. However, researchers did notice an overall increase in the diversity of T cells and the multiplication of specific cells geared toward recognizing tumor markers. The researchers caution that these findings are highly early-stage. The study looked at a very small group of just five patients at a single post-treatment point in time, meaning more research is needed to fully map out this complex immune response.

PubMed · 2 min read