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Ibrexafungerp: A novel antifungal

Ibrexafungerp is the first representative of a novel class of structurally-distinct glucan synthase inhibitors, triterpenoids.

It has broad spectrum activity encompassing Candida, Aspergillus, Pneumocystis, Dimorphic fungi and mucorales, including multi-drug resistant (MDR) species and pan resistant species such as Candida auris. Ibrexafungerp combines the well-established activity of glucan synthase inhibitors with the flexibility of oral and IV formulations, offering a broad use across different settings (in-patient and out-patient).

Ibrexafungerp has the potential to be an essential therapy in the treatment of multiple serious fungal infections:

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


  • Broad spectrum (including multidrug-resistant strains)

    Fungicidal vs. Candida

  • Convenient oral dosing

  • High tissue penetration

    High concentrations in tissues of interest, except CNS

  • Favorable safety profile and well tolerated

    ~2,000 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

Ibrexafungerp is an investigational drug. Items listed above illustrate ibrexafungerp target attributes.

How does ibrexafungerp work?

Ibrexafungerp 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
  • 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
  • Due to the different structure and enzyme-inhibition properties, ibrexafungerp retains activity against the majority of echinocandin-resistant strains
  • Disruption of the fungal cell wall is fungicidal against Candida spp
  • No cross-resistance with azoles because of the different MOA

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)
  • Retained activity at vaginal pH (4.5)
  • Synergistic antifungal activity when combined with azoles or polyenes, particularly relevant for the treatment of invasive aspergillosis

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