spec sheet12 rows
Belinostat is an intravenous pan-HDAC inhibitor of the hydroxamic-acid type; "pan" means it blocks the HDAC family broadly rather than one class. It won accelerated approval for relapsed or refractory peripheral T-cell lymphoma (PTCL), an aggressive and hard-to-treat group of lymph-node cancers of T cells, on the strength of a single-arm registration trial. It sits alongside romidepsin and belinostat's oral cousins as part of the small group of HDAC inhibitors that carved out a niche specifically in T-cell lymphoma.
- Pan-HDAC inhibitor active in T-cell lymphoma
- Durable responses in some relapsed/refractory patients
- Generally manageable toxicity in trials
- Fewer CYP drug-interaction dose changes than some peers
- Nausea and vomiting
- Fatigue and fever
- Anemia and low blood counts
- Possible QT / liver effects
Mechanism
Like the rest of the class, belinostat works by keeping enzymes from stripping acetyl groups off histones and other proteins; the acetyl marks build up, tightly packed chromatin loosens, and genes that the cancer had switched off, including ones that drive differentiation and apoptosis (programmed cell death), come back on, halting growth and killing the tumor cell [1][2]. Several enzymes are over-expressed in T-cell lymphomas, which helps explain why this class hits those diseases relatively hard, though the full reason for the T-cell preference is still debated [3].
The pivotal evidence is the BELIEF (CLN-19) trial, a single-arm phase II study in relapsed or refractory PTCL. Belinostat given as a daily infusion produced an overall response rate of about 26 percent, including complete responses, with some responses lasting well over a year, and it did this with a manageable toxicity profile dominated by nausea, fatigue, fever, and low blood counts; those results earned the FDA approval [4][5]. Reviews note a practical advantage in its handling: belinostat is cleared mainly by the liver enzyme UGT1A1, and no routine dose change was recommended for co-administered CYP inhibitors or inducers, though people with reduced UGT1A1 function need caution [6]. It remains one treatment option among several for this poor-prognosis disease rather than a cure.
receptor fingerprint
family (pan)inhibits broadly
Lymphoma cell apoptosis / differentiationpromotes
Safetyrisks and cautions, not medical advice
Belinostat is an intravenous cancer drug and a serious agent. The most common problems in trials were nausea and vomiting, fatigue, fever, anemia, and other low blood counts; as an HDAC inhibitor it also carries the class concerns about heart-rhythm (QT) effects and electrolyte balance, and severe liver and blood toxicities are possible. Because it is broken down by UGT1A1, patients with a genetic reduction in that enzyme (as in Gilbert syndrome) may need a lower dose. It is used only under oncology supervision; there is no non-clinical use for it.
Interactionsdocumented pairs only, not exhaustive
Belinostat is cleared mainly by UGT1A1 glucuronidation, and that single narrow pathway is where its interactions live. Strong UGT1A1 inhibitors such as atazanavir, nilotinib and several other tyrosine kinase inhibitors raise belinostat exposure and with it the risk of myelosuppression. Reduced-function UGT1A1 genotypes, UGT1A1*28 in particular, are genetic rather than pharmacological but have the identical consequence.
Belinostat and its metabolites inhibit CYP2C8 and CYP2C9 in vitro, which predicted a warfarin interaction that then failed to appear: a dedicated clinical study found no increase in AUC or Cmax for either R-warfarin or S-warfarin when the two were given together. It is a useful reminder that an in vitro signal is a hypothesis, not a finding. Belinostat does inhibit UGT enzymes, so exposure to other UGT substrates could rise, though that remains theoretical rather than documented in patients.
Additive myelosuppression with other cytotoxic chemotherapy is the plainer, more practical concern.
Checking a whole stack? Run it through interactions + stacks.
Subjective profileweighing the evidence above
An oncology infusion drug for relapsed T-cell lymphoma, used under specialist supervision and nowhere else. It buys durable responses in some patients at the cost of nausea, fatigue, low blood counts and possible QT and liver toxicity. There is no off-label or wellness use for this.
Resources
This entry is here for reference.
Research
- 2014first citedBelinostat for the treatment of peripheral T-cell lymphomas
- 2024most recentThe effect of liver dysfunction on the pharmacokinetic disposition of belinostat and its five m…
- 1.Belinostat in Patients With Relapsed or Refractory Peripheral T-Cell Lymphoma: Results of the Pivotal Phase II BELIEF (CLN-19) Study
- 2.Belinostat for the treatment of relapsed or refractory peripheral T-cell lymphoma
- 3.Belinostat in patients with refractory or relapsed peripheral T-cell lymphoma: a perspective review
- 4.Belinostat for the treatment of peripheral T-cell lymphomas
- 5.Profile of belinostat for the treatment of relapsed or refractory peripheral T-cell lymphoma
- 6.The effect of liver dysfunction on the pharmacokinetic disposition of belinostat and its five metabolites in patients with advanced cancers
6 listed here; entry last updated July 2026
Reviews
My notesprivate to this device
FAQ
How is belinostat given?
By intravenous infusion, typically over several consecutive days in a repeating cycle, in an oncology clinic. It is not an oral drug.
What is it approved for?
Relapsed or refractory peripheral T-cell lymphoma, based on the single-arm BELIEF trial that showed roughly a quarter of patients responded, some for over a year.
Why do HDAC inhibitors work in T-cell lymphoma?
Several HDAC enzymes are over-expressed in these cancers and the cells appear unusually dependent on them, so blocking HDACs hits T-cell lymphoma harder than many other tumors. The complete explanation is still being worked out.
Does my genetics matter for dosing?
It can. Belinostat is cleared by the liver enzyme UGT1A1, so people with a reduced-function version of that enzyme may need a lower dose to avoid extra toxicity.
Adverse effects
- Nausea and vomiting
- Fatigue and fever
- Anemia and low blood counts
- Possible QT / liver effects