DM199 for IgA Nephropathy (IgAN)

Improve Overall Kidney Function and Fight Autoimmunity.

DM199 (KLK1) is believed to improve overall kidney function via local stimulate the production of nitric oxide and prostaglandins, which help to improve renal blood flow and reduce inflammation. DM199 may also dampen the autoimmune component of IgAN by increasing the production of regulatory Tcells (Tregs), which are believed to help fight against autoimmunity.


Program Asset Route of Admin Development Stage
Preclinical Phase 1 Phase 2 Pivotal
IgA Nephropathy DM199 SC
REDUX Phase 2 Preclinical complete
Phase 1 complete
Phase 2 in progress
Pivotal not started

About IgA Nephropathy (IgAN)

IgA nephropathy (IgAN), is a progressive autoimmune disease that causes chronic inflammation of the kidney. Up to half of all IgAN cases will progress to end-stage renal disease (ESRD).

It is the most common cause of glomerulonephritis, an inflammatory disease that impairs the kidney’s ability to filter waste and excess water from the blood. Glomerulonephritis is a leading cause of ESRD after diabetes and is responsible for 25-30% of all annual ESRD cases.

Market Need

  • Rare disease which causes CKD by damaging the glomerulus
    • IgA antibody complex build-up causes inflammation
  • Affects 140,000 in U.S., 200,000 in E.U. and over 2 million in China
  • 50% of cases progress to end stage renal disease within 10-20 years
  • Limited FDA approved therapies available

Mechanism of Action

Potential Benefits of DM199 for IgAN

  1. Regulate blood flow:

    • Improve micro vascularization
    • Increases oxygen and nutrients
  2. Improve glomerular function:

    • Reduce inflammation, oxidative stress and fibrosis
    • Prevent or reduce thickening of glomerular basement membrane
    • Inhibit mesangial cell proliferation
  3. Increase T-regs (CKD autoimmune diseases)

    • Halt pathological autoimmune attack on glomerulus

Clinical Studies

We are currently conducting a Phase 2 trial of DM199 in patients with confirmed IgA nephropathy.

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