SCYNEXIS, Inc.

SCYNEXIS
Research Platform

Ibrexafungerp: An Innovative Antifungal

Our research platform has produced the first representative of a novel triterpenoid IV/oral antifungal family.

  • Novel glucan synthase inhibitor
  • Potent activity against most common fungi pathogens, including those resistant to other antifungals

“Ibrexafungerp–with its unique attributes such as extensive tissue distribution, broad spectrum of activity including Candida spp., Aspergillus spp. and Pneumocystis spp., activity against fungal strains resistant to other antifungals and its oral/IV flexibility–has the potential to overcome many of the limitations of current antifungal options and positively impact the life of patients suffering from these devastating infections.”

- David Angulo, M.D., Chief Medical Officer

Highlights

Product attributes supported by strong scientific evidence*

Broad Spectrum (including Multidrug-Resistant Strains)

Fungicidal vs. Candida

Flexible Oral/IV Dosing

Validated Mechanism of Action

Mininal off-target effects
Differentiated binding vs. echinocandins

High Tissue Penetration

High concentrations in lung and vaginal tissue

Safe and Well-Tolerated

1000+ subjects exposed Low risk of drug-drug interactions

Worldwide Rights and Long Exclusivity (Patent Protection up to 2035)

Qualified Infectious Disease Product (QIDP), Fast Track and Orphan Drug status for Invasive Candidiasis and Aspergillosis

QIPD and Fast Track status for Vulvovaginal Candidiasis

Ibrexafungerp (formerly SCY-078) is an investigational drug. Items listed above illustrate ibrexafungerptarget attributes.
*"strong scientific evidence" includes pre-clinical and clinical trial results.

How Does Ibrexafungerp Work?

Ibrexafungerp (formerly SCY-078 is a glucan synthase inhibitor and operates via a validated mechanism of action (MOA) that inhibits the enzyme responsible for the synthesis of β-(1,3)-glucan:

  • Inhibition of the synthesis of β-(1,3)-D-glucan, an essential component of the fungal cell wall of many pathogenic fungi, results in cytological and ultrastructural changes in the fungi compromising their ability to survive
  • Disruption of the fungal cell wall is fungicidal against Candida spp
  • The cell wall of fungi is a unique target not encountered in mammalian cells, which provides for the good safety profile of ibrexafungerp and other glucan synthase inhibitors (limited risk for "off-target" effect, such as human cell toxicity)
  • The MOA (glucan synthase inhibition) has been previously validated as a clinically relevant target by the echinocandins
  • No cross-resistance with azoles because of the different MOA
  • Due to the different structure and enzyme-inhibition properties, ibrexafungerp retains activity against the majority of echinocandin-resistant strains

How is Ibrexafungerp Different?

The structure of ibrexafungerp (formerly SCY-078) and echinocandins are very different, allowing for:

  • Different enzyme-inhibition properties than the echinocandins
  • Most gene mutations (FKS) that confer resistance to echinocandins do not affect the activity of ibrexafungerp
  • Administration orally and IV (echinocandins are only available IV)
  • Extensive distribution into key tissues associated with fungal infections, often achieving tissue concentration severalfold above the plasma concentrations (echinocandins have a limited tissue distribution achieving tissue concentration at or below plasma concentrations)

The MOA of ibrexafungerp is different from the azoles and polyenes, allowing for:

  • Retention of activity against azole and polyene-resistant strains
  • Potential for more favorable safety profile
  • Lower risk for drug-drug interaction (vs. azoles)
  • Enhanced activity at vaginal pH (4.5)
  • Synergistic antifungal activity when combined with azoles or polyenes, particularly relevant for the treatment of invasive aspergillosis.