Labyrinth therapy drugs show potential for Ottawa's highest asset for $800 million

An experimental maze treatment drug increases the urinary excretion of compounds that are biological indicators of metabolic diseases. Early clinical trial results show that the molecule has the best first-class potential in rare diseases, with few treatment options, and the opportunity to introduce new approaches to chronic kidney disease.
The placebo-controlled phase 1 test recruited 112 healthy adults and evaluated a range of study drugs MZE782. The main goal is to measure safety and tolerance, and the results reported on September 11 maze showed no serious adverse events or treatment-related complications, resulting in disruption to the study drug. The secondary and exploratory endpoints of the trial included urine measurements and measures of renal function. These results excited investors.
MZE782 of the maze is a small molecule designed to selectively inhibit SLC6A19, the gene code is a transporter, which plays a key role in the intestinal and kidney absorption of phenylalanine, an amino acid found in certain foods. A rare disease that the maze is designed to treat is bencocoa proteinuria, where phenylalanine accumulates in the body and causes cognitive and behavioral problems. This accumulation is caused by genetic defects in the enzymes required to break down amino acids. Benzoneuria is mainly managed through dietary changes to limit phenylalanine intake. Bioagents Drug Market Two FDA-approved drugs for rare diseases.
The phase 1 results of the maze drug show dose-dependent excretion of phenylalanine and glutamine. The maze said that the excretion of these amino acids was higher, confirming that MZE782 was involved and inhibited SLC6A19. A single dose of MZE782 at 960 mg resulted in 39 times urinary excretion of phenylalanine within 24 hours. The company also said that on Day 7, a 42-fold increase in urine excretion of amino acids was observed in the group receiving the 240 mg twice a day dose of 240 mg of the study drug.
Multiple peers in the study also evaluated the estimated glomerular filtration rate (EGFR), a measure of how the kidneys filter blood. MZE782 results in a dose-dependent decrease in EGFR within 7 days, similar to those observed for SGLT2 and RAAS inhibitors, and two classes of drugs are currently used to treat chronic renal disease. Maze says that using other renal medications, this initial inclination is associated with a slower decline in EGFR in patients with chronic kidney disease and better renal function in patients with chronic kidney disease.
Thanks to the results of Phase 1, Maze says it is now planned to advance MZE782 to two proof-of-concept Phase 2 clinical trials. The phenyl ketone study will measure the decrease in phenylalanine in the blood. Chronic renal disease studies will measure a decrease in urine protein indicating the disease. Both studies are expected to begin in 2026.
Leerink Partners analyst Joseph Schwartz said in a note sent to investors that the increase in phenylalanine excretion not only surpassed previously set target mazes, but also surpassed the measures achieved by JNT-57, a major asset for JNANA therapy. Otsuka Pharmaceutical has enough hope in the drug candidate to acquire Jnana for $800 million last year, with another $325 million linked to achieving milestones. The JNANA drug is currently under test for phase 3 in benzoneuria, but Schwartz sees the maze drug as a strong competitor to the disease and chronic kidney disease.
“In general, these results from the MZE782 of the Maze show first-class visibility in our opinion, and we think the program will start to gain more credibility from investors,” Schwartz said.
The maze follows data readings, with private locations raising $150 million, and $150 million from new and early investors. The biotech said the proceeds and their existing capital will be used to fund the planned MAZ782 test. Capital will also support a Phase 2 test of the maze state-of-the-art program MZE829, which is being developed for the treatment of patients with APOL1-mediated renal disease.
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