Subcutaneously Administered SIL204 Reduces Both Primary Tumors and Metastases in Clinically Relevant Orthotopic Models in Human Pancreatic Cancer Cells
Wednesday, March 5, 2025
CHromadex results, advances
Revenue: $29.1 million in Q4 2024, a 37% increase year-over-year.
Net Income: $7.2 million in Q4 2024.
Full Year Revenue: $99.6 million, a 19% growth year-over-year.
Full Year Net Income: $8.6 million, compared to a net loss of $4.9 million in 2023.
Cash Flow from Operations: $12.1 million in 2024.
Cash Balance: $44.7 million with no debt at year-end 2024.
Gross Margin: Improved by 150 basis points to 62.5% in Q4 2024.
E-commerce Sales: $17.3 million in Q4 2024, a 30% increase year-over-year.
NIAGEN Ingredient Sales: $5.3 million in Q4 2024, a 96% increase year-over-year.
Selling and Marketing Expense: Improved 90 basis points to 29.9% of net sales in Q4 2024.
General and Administrative Expenses: Decreased by $4.4 million in Q4 2024.
Operating Income: $7.1 million in Q4 2024, compared to a $200,000 operating loss in Q4 2023.
For the complete transcript of the earnings call, please refer to the full earnings call transcript.
Positive Points
ChromaDex Corp (NASDAQ:CDXC) reported record revenues of $29.1 million for Q4 2024, marking a 37% increase year-over-year.
The company achieved a net income of $7.2 million in Q4 2024, contributing to a full-year net income of $8.6 million, a significant turnaround from a net loss in 2023.
ChromaDex Corp (NASDAQ:CDXC) ended the year with $44.7 million in cash and no debt, indicating strong financial health.
The e-commerce channel experienced robust growth with net sales of $17.3 million, a 30% increase year-over-year.
The NIAGEN ingredients business saw a 96% increase in net sales year-over-year, driven by strong demand for both food-grade and pharmaceutical-grade products.
Negative Points
Supply chain issues delayed the availability of pharmaceutical-grade NIAGEN by two to three months, impacting sales.
The company faces challenges from competitors making false claims and infringing on patents, which could affect market share.
There is a need for more regulatory action from the FDA and FTC to prevent misleading practices by competitors.
General and administrative expenses are expected to increase by approximately $5 million to $6 million in 2025 due to business growth investments.
The company anticipates potential impacts from tariffs on international business, although they expect these to be minimal.
https://finance.yahoo.com/news/chromadex-corp-cdxc-q4-2024-071005949.html
Jazz Pharmaceuticals to Acquire Chimerix, Further Diversifying Oncology Portfolio
Dordaviprone addresses a significant unmet patient need for patients with rare, high-grade brain tumors-
-Transaction to add near-term commercial opportunity to Jazz's pipeline-
-Transaction represents total cash consideration of approximately $935 million, or $8.55 per share-
Tuesday, March 4, 2025
Li Ka-shing Escapes Trump Glare With $19 Billion, Soaring Stock
After a lifetime of dealmaking, 96-year-old Hong Kong billionaire Li Ka-shing may have just pulled off one of his boldest transactions yet.
Under pressure from the Trump administration over two ports at the Panama canal controlled by CK Hutchison Holdings Ltd., Li’s company announced a plan to sell off the bulk of global ports business to a consortium led by BlackRock Inc. In return, the Hong Kong firm will receive cash proceeds of more than $19 billion.
Bayer Expects Profits to Fall Again Amid Sluggish Farming Price
Bayer AG forecast a third straight year of falling profit as the German company struggles with mass litigation in the US, slumping prices for agriculture products and fresh competition for some of its best-selling medicines.
Core earnings will probably fall to between €4.50 ($4.78) and €5 a share on a constant-currency basis, the company said in a statement Wednesday. That’s down from €5.05 last year and compares with analysts’ average estimate of €4.61.
Trump wants to kill $52.7 billion semiconductor chips subsidy law
President Donald Trump said Tuesday U.S. lawmakers should get rid of a landmark 2022 bipartisan law to give $52.7 billion in subsidies for semiconductor chips manufacturing and production and use the proceeds to pay debt.
"The CHIPS act is a horrible, horrible thing. We give hundreds of billions of dollars and it doesn't mean a thing. They take our money and they don't spend it," Trump said in a speech to Congress. "You should get rid of the CHIPS Act and whatever is left over, Mr. Speaker, you should use it to reduce debt."
Scientists identify neural mechanism of leptin resistance in obesity—and how to reverse it
Worldwide obesity rates have more than doubled since 1990, with nearly a billion people now falling into the category. Though a complex interplay of genes, diet, and environment contribute, 90% of cases share one thing in common: leptin resistance.
In lean individuals, fat cells produce the hormone leptin, which suppresses appetite. But in most individuals with obesity, this signal fails to register. Why this happens has been a mystery for more than three decades, ever since Jeffrey M. Friedman's laboratory at the Rockefeller University cloned the leptin gene in 1994.
But now Bowen Tan, Kristina Hedbacker, and other researchers in Friedman's Laboratory of Molecular Genetics have discovered a neural mechanism involved in leptin resistance—and, crucially, a way to reverse it in mice using a well-known drug.
As the researchers describe in a paper in Cell Metabolism, the drug rapamycin restores leptin sensitivity to diet-induced obese mice, leading to significant loss of fat with only minimal effects on muscle.
"Before our research, the cause of obesity in diet-induced obese mice was unknown, leaving a critical gap in our understanding of how leptin resistance develops and how it can be reversed," says Tan, co-first author and a graduate student in Friedman's lab.
"Even though Jeff Friedman discovered this powerful hormone back in 1994, its full potential to help people lose weight hasn't been realized because most obese patients have acquired resistance to leptin," says co-first author Hedbacker, a research specialist at HHMI and a member of Friedman's lab. "It's really exciting to think that there may be means for addressing this."
Too much of a good thing
Long before plant agriculture and animal domestication provided more reliable access to nutrients, humans routinely faced starvation. That's when the leptin circuit evolved.
Neurons in the hypothalamus—the brain's energy-balance regulator—pick up satiety signals from fat, which secretes leptin; a high amount of the hormone signals that there are adequate fat stores and the energy tank is full, while a low leptin level indicates that the body is running on fumes.
Our brains retain this system for regulating food consumption, even as conditions around it have drastically changed, with more people having access to high-calorie foods than ever before. Data suggest that as weight is gained and leptin levels continually rise, the brain gradually stops responding to leptin.
"This phenomenon is analogous to insulin resistance, which is the most common cause of diabetes and a condition that develops over time, due, in part, to chronically elevated insulin levels," Hedbacker says.
"Similarly, most people with obesity have high leptin, but reception of their leptin signaling is blocked. This makes it very difficult to lose weight, because the brain does not receive the appropriate signal of how much fat is stored."
With this in mind, Tan and Hedbacker set out to identify biomarkers in the 10% of patients with obesity who are leptin sensitive and could potentially benefit from leptin treatment. They looked in both leptin-sensitive and leptin-resistant mice.
What they discovered sent them down an unexpected path. They found that in leptin-resistant mice, the levels of two essential amino acids are dysregulated in response to leptin. These two amino acids, methionine and leucine, are known activators of a signaling molecule called mTOR (short for "mammalian target of rapamycin"). Leptin-sensitive animals showed no such dysregulation.
"With this as a starting point, we found that mTOR is hyperactive in specific brain regions and cell types in obese animals," Tan says.
Weight loss
To investigate further, the researchers tested the effects of rapamycin, an mTOR inhibitor, in four groups of mice: leptin-sensitive mice fed a low-calorie chow diet, mimicking people who remain lean; mice fed a high-fat diet that developed leptin resistance, similar to people who develop obesity; and two sets of obese mice that were leptin deficient but responsive to the hormone. These mice were fed either the low-calorie chow diet or the high-fat diet.
The results were striking: "Obese mice fed a high-fat diet and treated with the mTOR inhibitor rapamycin lost significant amounts of weight, which—similar to leptin treatment in leptin-sensitive animals—was primarily due to a decrease in the amount of adipose tissue," Tan says.
Loss of fat mass without muscle mass is characteristic of leptin treatment, but it's unusual for weight loss in general. For example, weight loss achieved by dieting or treatment with highly effective anti-obesity medications such as Ozempic leads to a significant loss of both fat and muscle.
They then investigated which cell types in the brain were the target of rapamycin, focusing on a dozen cell types in the hypothalamus, where leptin is known to act. Using single-cell sequencing, Tan found that rapamycin treatment exerted significant effects on neurons in the hypothalamus that express a gene known as POMC. These neurons are known to mediate leptin's weight-reducing effects.
"We found that rapamycin reduced mTOR in POMC neurons and restored their receptivity, essentially resensitizing the animals to leptin and leading to a decreased size of fat depots relative to muscle mass," Hedbacker says.
Defects in POMC-expressing neurons are also known to cause leptin resistance and obesity, Friedman notes, adding, "it was satisfying to find that an acquired form of leptin resistance targets this same pathway."
By showing that it is possible to restore leptin signaling, the findings could potentially lead to new obesity treatments. Future research in Friedman's lab will explore why a high-fat diet elevates mTOR signaling in the brain.
The lab will also try to develop means for inhibiting mTOR specifically in POMC neurons to avoid potential side effects of systemic rapamycin use, which is linked to glucose intolerance and potentially diabetes.
More information: A Cellular and Molecular Basis of Leptin Resistance, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.01.001. www.cell.com/cell-metabolism/f … 1550-4131(25)00001-4
https://medicalxpress.com/news/2025-03-scientists-neural-mechanism-leptin-resistance.html
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