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Our Science

Our Science

Intraocular pressure is comprised of four distinct components that, combined, lead to total intraocular pressure (IOP). These four components are currently best described by the modified Goldmann equation, which includes contributions from the Aqueous Humor Inflow Rate (Q), Uveoscleral Outflow Rate (U), Conventional Outflow Facility (C), and Episcleral Venous Pressure (EVP). EVP is the largest component of IOP, contributing around 2/3 of total IOP. However, no approved therapy to date solely targets EVP.

Modified Goldmann Equation for IOP

Aqueous Humor Inflow Rate

Beta Blockers:
  • Timolol
  • Betaxolol
  • Levobunolol
  • Metipranolol
Alpha Agonists:
  • Brimonidine
  • Apraclonidine
Carbonic Anhydrase Inhibitors:
  • Brinzolamide
  • Dorzolamide
  • Acetazolamide
  • Methazolamide

Uveoscleral Outflow Rate

Prostaglandin Analogs:
  • Latanoprost
  • Bimatoprost
  • Travaprost
  • Tafluprost
  • Latanoprostene bunod
Alpha Agonists:
  • Brimonidine
  • Apraclonidine

Conventional Trabecular Outflow Facility

Cholinergics (Miotics):
  • Pilocarpine
  • Carbachol
Rho Kinase Inhibitors:
  • Netarsudil

Episcleral Venous Pressure

Specifically targeted by QLS-101

Our Pipeline

Discovery Pre-clinical IND-Enabling Phase 1 Phase 2 Phase 3 Approval
QLS-101*POAG/OHT
Phase 2
QLS-101*NTG
Phase 1
QLS-101*SWS
Phase 1
QLS-700SR-IOP
Discovery
QLS-700Neuroprotection
Discovery
*Worldwide Rights Exclusive License from Mayo Clinic

QLS-101

QLS-101 is our lead program based upon research from the laboratory of Professor Michael Fautsch at Mayo Clinic. The original compounds were first synthesized at the laboratory of Professor Peter Dosa at the University of Minnesota.

QLS-101 is a novel prodrug of a well-characterized ATP-sensitive potassium (KATP) channel modulator that lowers intraocular pressure (IOP) by relaxing vessels of the vascular and vascular-like tissues distal to the Trabecular Meshwork, thereby reducing distal outflow resistance and lowering Episcleral Venous Pressure (EVP).

Though multiple mechanisms of action exist to lower IOP in patients with glaucoma, these agents all target only 3 of the 4 components of IOP as described by the Goldmann equation for IOP: the Aqueous Humor Inflow Rate (Q), Uveoscleral Outflow Rate (U), or Conventional Outflow Facility (C). There are currently no approved drugs that solely target the reduction of EVP. This leaves a significant gap in the potential to maximally lower IOP since EVP can be the largest determinant of overall IOP.

QLS-101 has shown efficacy in lowering IOP across multiple preclinical animal species, including mice, rabbits, dogs, and non-human primates, as well as in human eye explants. To date, QLS-101 has been demonstrated to be well-tolerated with no observed hyperemia in the efficacious dose range.

By uniquely targeting EVP and distal outflow, QLS-101 enables the treatment of diseases for which there are currently inadequate therapies: namely, those diseases of pathologic EVP or where EVP currently sets the floor for maximal therapy despite the use of multiple agents since no approved drugs currently lower EVP primarily.

Qlaris Bio has initiated clinical studies with QLS-101 in patients with Primary Open Angle Glaucoma, Ocular Hypertension, Normal Tension Glaucoma, and Sturge-Weber syndrome.

Clinical Trials

QLS-101 in Primary Open Angle Glaucoma and Ocular Hypertension

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QLS-101 in Normal Tension Glaucoma

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QLS-101 in Adults with Sturge-weber Syndrome

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