Congruence Therapeutics Announces Oral Presentation on CGX-195, a Novel Small Molecule AAT Corrector, at the ERS Alpha-1 Antitrypsin (AAT) Conference 2026
– CGX-195 increased functional, secreted Z-A1AT and reduced polymerized Z-A1AT in cellular assays and in the PiZ mouse model –
MONTREAL, Oct. 23, 2026 /PRNewswire/ -- Congruence Therapeutics ("Congruence"), a clinical-stage, computationally driven biotechnology company building a pipeline of pharmacological correctors for genetically validated, difficult-to-drug targets, today announced an oral presentation at the European Respiratory Society (ERS) Alpha-1 Antitrypsin Conference 2026, held in collaboration with the European Alpha-1 Research Collaboration (EARCO), October 23–24, 2026, in Barcelona, Spain.
Congruence scientists will present preclinical data on CGX-195 (CO-8195), the Company's novel, orally active small molecule corrector for alpha-1 antitrypsin deficiency (AATD), describing the activity of CGX-195 in cellular assays and in the PiZ transgenic mouse model of AATD. CGX-195 increased levels of functional, secreted Z-A1AT and reduced levels of polymerized Z-A1AT, which the Company believes addresses AATD at its root cause.
"We are honored that our preclinical results with CGX-195 were selected for a podium presentation at the field's leading scientific meeting on alpha-1 antitrypsin deficiency," said Sharath Hegde PhD, Chief Scientific Officer of Congruence. "By correcting the misfolding of the Z variant at its source, an oral small molecule like CGX-195 has the potential to address both liver and lung manifestations of this disease: restoring circulating, functional A1AT to protect the lung while reducing the toxic polymer burden in the liver. These data further validate our Revenir™ platform's ability to design correctors for difficult-to-drug misfolded proteins, and we look forward to advancing CGX-195 toward the clinic in 2027."
Oral Presentation Details:
- Title: CO-8195, a novel orally active small molecule corrector for Alpha-1 Antitrypsin Deficiency (AATD), increases functional secreted Z-A1AT and reduces polymerized Z-A1AT in cellular assays and in the PiZ mouse model
- Abstract number: OP01
- Session: Oral Presentations (Chairs: Didier Cataldo and Jeanine D'Armiento)
- Presenter: Anzhelika Kabro, Senior Director, Chemistry, Congruence Therapeutics
- Date and time: Friday, October 23, 2026, 16:50–17:00 CEST (10:50–11:00 a.m. ET)
- Location: ERS Alpha-1 Antitrypsin Conference 2026, Barcelona, Spain
About Alpha-1 Antitrypsin Deficiency (AATD)
Alpha-1 antitrypsin deficiency is an inherited disorder caused by mutations in the SERPINA1 gene, which encodes alpha-1 antitrypsin (A1AT), a protease inhibitor produced mainly in the liver that protects the lung from damage by neutrophil elastase. The most common severe variant, the Z mutation (Glu342Lys), causes A1AT to misfold and polymerize within liver cells. This produces two forms of disease: insufficient circulating A1AT leaves the lungs exposed to protease damage, leading to early-onset emphysema and COPD, while accumulation of polymerized protein in hepatocytes can cause liver fibrosis, cirrhosis and hepatocellular carcinoma. Currently available augmentation therapy requires weekly intravenous infusions and does not address the liver disease, leaving a significant unmet need for therapies that correct the underlying misfolding.
About CGX-195
CGX-195 is a novel, orally active small molecule corrector of Z-A1AT discovered using Congruence's proprietary Revenir™ computational platform. CGX-195 is designed to bind and stabilize the misfolded Z variant of A1AT, promoting its proper folding and secretion as functional protein while reducing the formation of toxic polymers in the liver. In preclinical studies, CGX-195 increased functional secreted Z-A1AT and reduced polymerized Z-A1AT in cellular assays and in the PiZ mouse model. Congruence is completing IND-enabling activities for its AATD program, with the goal of advancing CGX-195 toward the clinic in 2027.
About Congruence Therapeutics
Congruence is a clinical-stage, computationally driven biotechnology company addressing diseases at their structural source by designing oral small molecules that correct the underlying protein defects associated with genetically validated diseases, including MC4R-deficient genetic obesity, alpha-1 antitrypsin deficiency, and GBA-driven Parkinson's disease. Our proprietary Revenir™ platform models protein structure and dynamics at the atomic level to identify small molecules capable of restoring normal protein function. The company is also advancing multi-target research collaborations with large pharmaceutical companies across additional therapeutic areas. For more information, visit www.congruencetx.com.
Contacts
Company
Charles Grubsztajn
Chief Operating Officer
Congruence Therapeutics
cgrubsztajn@congruencetx.com
Investor
Hanna Erdtmann
Senior Associate
astr partners
hanna.erdtmann@astrpartners.com
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