Target intelligence / Profile preview

Fungal ergosterol biosynthesis enzyme

Molecular classification
Enzyme (specifically, multiple enzymes of the sterol/ergosterol biosynthesis metabolic pathway)[1][4][5].
01

Overview

The term "fungal ergosterol biosynthesis enzyme" refers to any of the suite of enzymes involved in the multi-step pathway that produces **ergosterol**, the principal sterol in fungal cell membranes. Ergosterol is essential for the structural integrity, fluidity, and viability of fungal cells and plays a key role in fungal growth and pathogenesis. The pathway includes over 20 enzymes catalyzing reactions from squalene (mevalonate pathway) to ergosterol via intermediates such as lanosterol and zymosterol. Key enzymes in this process include **lanosterol 14α-demethylase** (Cyp51/Erg11), **squalene epoxidase** (Erg1), **sterol C-8 isomerase** (Erg2), **sterol C-5 desaturase** (Erg3), **sterol C-24 methyltransferase** (Erg6), among others. These enzymes are major targets of clinically important antifungal drugs, with azoles targeting Cyp51, allylamines targeting Erg1, and morpholines inhibiting Erg2. Inhibiting ergosterol synthesis disrupts membrane function and causes fungal death or stasis. Drug resistance often arises from mutations or regulatory changes in these enzyme genes[1][2][4][7]. Despite multiple essential enzymes in the pathway, the term itself is non-specific; structured databases and medical literature usually reference targets by the specific enzyme, such as "Lanosterol 14α-demethylase (Cyp51/Erg11)."[1][4]. Important note: - It is **not** a single canonical molecule or target but refers to a multi-enzyme pathway with many possible specific targets (e.g., Erg11p, Erg1p, Erg2p, etc.)[1][4]. - For precise drug discovery or clinical purposes, the **exact enzyme (like "lanosterol 14α-demethylase") should be specified** rather than the pathway in general. - The current label is **too broad and non-specific** to map directly to existing databases without additional clarification. In summary: "Fungal ergosterol biosynthesis enzyme" is not a unique molecular entity but a general term for any enzyme in the ergosterol biosynthetic pathway in fungi, most notably including lanosterol 14α-demethylase (Cyp51/Erg11), squalene epoxidase (Erg1), and others, which are major antifungal drug targets due to their essential role in fungal membrane synthesis[1][4][7].

Other names
Individual enzymes include Lanosterol 14α-demethylase (also known as Erg11 or Cyp51), Squalene epoxidase (Erg1), Sterol C-8 isomerase (Erg2), C-24 methyltransferase (Erg6), C-5 sterol desaturase (Erg3), C-22 sterol desaturase (Erg5), C-24 sterol reductase (Erg4), and others[1][2][4][5].Collectively sometimes called ergosterol pathway enzyme, erg genes, ergosterol biosynthetic enzymes.
02

Mechanism of action

Inhibition of specific ergosterol biosynthetic enzymes, leading to depletion of ergosterol and accumulation of toxic sterol intermediates, which compromises fungal cell membrane integrity and function[1][4][7]. Direct binding to ergosterol in fungal membranes (for polyenes such as amphotericin B), forming pores and causing cell death[6].

03

Biological functions

Fungal cell membrane synthesis[1][4].Membrane fluidity and permeability regulation[4][5].Maintenance of fungal cell viability[1][4].Fungal pathogenesis and virulence[1][6].Drug resistance (role in antifungal resistance mechanisms)[1][4].
04

Disease associations

Infection (targeted in antifungal therapy against pathogenic fungi such as Candida, Aspergillus, Cryptococcus)[1][4][6].Antifungal drug resistance[1][2].
05

Safety considerations

Potential toxicity to human cells if drugs cross-react with cholesterol biosynthesis enzymes (most antifungals are selective, but side effects still occur—e.g., hepatotoxicity of azoles)[4].Drug resistance due to overexpression, mutation, or regulation of ergosterol pathway genes[1][2].Limited selectivity can restrict pharmacological window[7].Some antifungals (e.g., amphotericin B) associated with nephrotoxicity[6].
06

Interacting drugs

Azole antifungals (e.g., fluconazole, itraconazole, voriconazole—target Erg11/Cyp51/Lanosterol 14α-demethylase)[1][4][6].

3 more in the full profile.

07

Biomarkers

Expression or mutation of *ERG11/CYP51* gene (lanosterol 14α-demethylase) for azole resistance[1].Accumulation of sterol pathway intermediates detectable by mass spectrometry, which can indicate pathway inhibition[1][4].Fungal susceptibility tests using specific inhibitors[1][4].

Beyond the preview

Go deeper on Fungal ergosterol biosynthesis enzyme.

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Fungal ergosterol biosynthesis enzyme.

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call