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Disease

Oligodendroglioma

Late-stage therapeutic developmentEmerging researchRising momentum
3
Publications
22
Clinical trials
3
Related conditions
1
Related proteins
2025
Latest publication
Current focus
Isocitrate dehydrogenase biologyTherapeutic developmentGenetics & risk factors
Latest activity
beta

Recent clinical, regulatory, research and industry developments relating to this disease.

FDA Approval Summary: Vorasidenib for IDH-Mutant Grade 2 Astrocytoma or Oligodendroglioma Following Surgery.

Research2025-11-01Clinical cancer research : an official journal of the American Association for Cancer Research

Approval: Voranigo (EMA)

Regulatory2025-09-17EMA

What's happening now

An analyst briefing on current research, clinical, regulatory and industry activity surrounding this disease.

Major developments
Important regulatory approvalImportant
Voranigo as monotherapy is indicated for the treatment of predominantly non‑enhancing Grade 2 astrocytoma or oligodendroglioma with an IDH1 R132 or IDH2 R172 mutation in adult and adolescent patients aged 12 years and older and weighing at least 40 kg who only had surgical intervention and are not in immediate need of radiotherapy or chemotherapy (see section 5.1).2025-09-17
Research Highlights1View
Clinical Milestones5View
Regulatory Updates1View
  • 2025-09-17Approval — VorasidenibVoranigo as monotherapy is indicated for the treatment of predominantly non‑enhancing Grade 2 astrocytoma or oligodendroglioma with an IDH1 R132 or IDH2 R172 mutation in adult and adolescent patients aged 12 years and older and weighing at least 40 kg who only had surgical intervention and are not in immediate need of radiotherapy or chemotherapy (see section 5.1).
Activity timeline7

Therapeutic landscape

Therapies with a regulatory footing for this condition, alongside the wider set of agents co-studied with it in the literature.

Approved & established therapies
Vorasidenibapproved

Approval — Voranigo as monotherapy is indicated for the treatment of predominantly non‑enhancing Gra… (2025)

Clinical trials

18 sponsors · 1 new · 0 completed in the last 12 months (net +1)

The current development programme across all trial phases.

Clinical programme
22
All trials
6
Active
3
Late-stage
6
Completed
Recruiting
Recently completed

Regulatory timeline

Drug regulatory events matched to this condition by indication — EMA.

First approvals
2025emaApprovalVorasidenib· Voranigo as monotherapy is indicated for the treatment of predominantly non‑enhancing Grade 2 astrocytoma or oligodendroglioma with an IDH1 R132 or IDH2 R172 mutation in adult and adolescent patients aged 12 years and older and weighing at least 40 kg who only had surgical intervention and are not in immediate need of radiotherapy or chemotherapy (see section 5.1). source ↗

European Medicines Agency (CC BY 4.0). Events are matched to this condition by drug indication text — approvals/updates for drugs indicated for it, not disease-specific acts.

Research activity

3 papers

Key research shaping understanding of this disease, combining the latest publications with the most influential evidence.

Publications over time
20052025
Most influential

IDH1 and IDH2 mutations in gliomas.

The New England journal of medicine · 2009 · 4,526 cites

Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

The New England journal of medicine · 2005 · 994 cites

FDA Approval Summary: Vorasidenib for IDH-Mutant Grade 2 Astrocytoma or Oligodendroglioma Following Surgery.

Clinical cancer research : an official journal of the American Association for Cancer Research · 2025 · 2 cites
Recent publications

FDA Approval Summary: Vorasidenib for IDH-Mutant Grade 2 Astrocytoma or Oligodendroglioma Following Surgery.

Clinical cancer research : an official journal of the American Association for Cancer Research · 2025 · 2 cites

IDH1 and IDH2 mutations in gliomas.

The New England journal of medicine · 2009 · 4,526 cites

Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

The New England journal of medicine · 2005 · 994 cites
Major themes6
  • Mutation2
  • Astrocytoma1
  • Brain Neoplasms1
  • Isocitrate Dehydrogenase1
  • Oligodendroglioma1
  • Triazines1
Leading journals2
  • The New England journal of medicine2
  • Clinical cancer research : an official journal of the American Association for Cancer Research1
Leading researchers8
  • Ananthula S1
  • Aungst SL1
  • Barbato MI1
  • Barone AK1
  • Batinic-Haberle I1
  • Beroukhim R1
  • Bhatnagar V1
  • Bi Y1
Affiliations (unnormalised)4
  • Center for Drug Evaluation and Research1
  • David Geffen School of Medicine at the University of California1
  • Oncology Center of Excellence1
  • Pediatric Brain Tumor Foundation Institute1

Disease biology

1 match

Key proteins & gene products studied in this disease. Number shows shared papers.

Related conditions

3 matches

Diseases frequently studied alongside this one. Number shows shared papers.

Reference

Authoritative identity, definition & identifiers.

Defined in MeSH

A relatively slow-growing glioma that is derived from oligodendrocytes and tends to occur in the cerebral hemispheres, thalamus, or lateral ventricle. They may present at any age, but are most frequent in the third to fifth decades, with an earlier incidence peak in the first decade. Histologically, these tumors are encapsulated, relatively avascular, and tend to form cysts and microcalcifications. Neoplastic cells tend to have small round nuclei surrounded by unstained nuclei. The tumors may vary from well-differentiated to highly anaplastic forms. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2052; Adams et al., Principles of Neurology, 6th ed, p655)

References & data sources
  • Disease identity & definition — NLM Medical Subject Headings (MeSH), public domain
  • Clinical trials — ClinicalTrials.gov (U.S. National Library of Medicine)
  • Research activity — Europe PMC (EMBL-EBI) + OpenAlex-derived paper links
  • Related entities are derived from literature co-mention (studied together) — associative, not causal.