Zucara Therapeutics Announces Publication of Preclinical Study Demonstrating the Ability of ZT-01 to Restore Glucagon Release in Type 1 Diabetes


PR Newswire

TORONTO, February 8, 2022

– ZT-01 Restored Glucagon Secretion and Reduced the Frequency and Severity of Hypoglycemia in a Preclinical Model of Insulin-Induced Hypoglycemia –

TORONTO, February 8, 2022 /PRNewswire/ – Zucara Therapeutics Inc., a diabetes life sciences company developing the first once-daily treatment to prevent insulin-induced hypoglycemia (low blood glucose), announced today today that the peer-reviewed journal, Diabetes, obesity and metabolismpublished a paper reporting positive preclinical data showing the effect and pharmacokinetics of ZT-01, which is currently in phase 1b proof-of-concept trial for the treatment of insulin-induced hypoglycemia in patients with type 1 diabetes (“T1D”).

The article, titled “ZT-01 – A Novel Somatostatin Receptor 2 Antagonist for Restoring the Glucagon Response to Hypoglycemia in Type 1 Diabetes”, was co-authored by members of Zucara Therapeutics in collaboration with Michael C. Riddell at York University and the lab of the main author Owen Chan to University of Utah. The study reports that ZT-01, a somatostatin 2 receptor (“SSTR2a”) antagonist, stimulates glucagon release and reduces hypoglycemia in rats with T1D. The study also compares the performance of the ZT-01 with an earlier SSTR2a prototype, the PRL-2903.

“We are delighted with the positive results of this preclinical study, the efficacy part of which used a methodology similar to that of our current phase. 1b clinical trial,” said Richard Ligins, scientific director of Zucara Therapeutics. “This study demonstrated that ZT-01 significantly increased glucagon secretion in rats with T1D and reduced the frequency and severity of hypoglycemia, suggesting the potential of ZT-01 to reduce exposure to T1D. hypoglycemia in humans with T1D.”

The results of the preclinical efficacy study demonstrate that ZT-01 was significantly more effective in preventing the onset of hypoglycemia than PRL-2903 and exhibited superior pharmacokinetic and pharmacodynamic properties when administered by injection under -cutaneous or intraperitoneal. When given one hour before induction of hypoglycemia, treatment with ZT-01 or PRL-2903 slows the onset and reduces the overall severity of hypoglycemia, but to varying degrees: treatment by PRL-2903 delays hypoglycemia – which for the purposes of this study was a drop in blood glucose concentration to 3.0 mM – by approximately 10 minutes compared to over an hour with ZT -01. Additionally, PRL-2903 failed to prevent blood glucose concentrations from reaching the same nadir (approximately 2.0 mM) as vehicle-treated animals. Mean blood glucose after ZT-01 treatment reached a nadir of 3.8 mM, with more than 60% of rats completely avoiding significant hypoglycemia below the 3.0 mM threshold.

Data show that the novel SSTR2a, ZT-01, exhibited greater exposure after subcutaneous administration compared to PRL-2903 and significantly increased glucagon secretion in rats with T1D,

an improvement in counter-regulation associated with a reduction in the severity and frequency of hypoglycaemia. These results suggest that antagonism of SSTR2 may be an appropriate therapeutic strategy to reduce exposure to hypoglycemia in humans with T1D. Zucara is currently leading a phase 1b proof-of-concept clinical trial in people with T1D, with results expected in Q2 2022.

The article is available at

About Zucara Therapeutics Inc.

Zucara Therapeutics is developing ZT-01, a first-in-class treatment to prevent insulin-induced hypoglycemia in patients using insulin therapy. ZT-01 is designed to inhibit somatostatin, a pancreatic hormone that impairs the glucagon response to hypoglycemia in people with insulin-dependent diabetes. ZT-01 restores glucagon secretion to prevent hypoglycemia, which could radically change diabetes management and improve both health and quality of life for patients. For more information, visit www.zucara.ca.


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SOURCE Zucara Therapeutics Inc.


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