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Romidepsin is an unusual HDAC inhibitor; instead of the small hydroxamate or benzamide chemistry of most drugs in this class, it is a bicyclic depsipeptide (a ring-shaped molecule made of both amino acids and an ester link) originally isolated from a soil bacterium. It behaves as a prodrug that only becomes active once inside the cell, and it prefers the class I HDACs. It was approved to treat T-cell lymphomas of the skin and, later, the lymph nodes and other tissues, though its use in the second setting has since narrowed after a confirmatory trial disappointed.
- Distinct bicyclic-peptide chemistry, self-activating inside cells
- Class I-preferring HDAC inhibition
- Durable responses in cutaneous T-cell lymphoma
- Eases the severe itch of skin lymphoma
- Nausea and vomiting
- Fatigue
- Low blood counts
- QT-interval / cardiac effects
Mechanism
Romidepsin arrives as an inactive, folded held shut by an internal disulfide bond. Once it is taken up by cells, the reducing environment inside snaps that bond open and frees a sulfur-bearing (thiol) arm; that arm reaches into the zinc-containing active site of the enzyme and jams it, giving strong, fairly class I-selective inhibition [1][2]. With the class I HDACs shut down, acetyl marks accumulate on histones, silenced genes switch back on, and the lymphoma cells stall and die by apoptosis (programmed cell death) [3].
In practice this translated into meaningful single-agent activity. Two phase II trials in relapsed or refractory cutaneous T-cell lymphoma showed durable responses in roughly a third of patients, with improvements in the maddening itch that comes with the disease, which supported its approval there [4]; parallel work extended it to peripheral T-cell lymphoma, where inhibitors as a group show a striking preference for T-cell disease that is still not fully explained [2][5]. The honest caveat is that a later combination trial adding romidepsin to standard chemotherapy in peripheral T-cell lymphoma failed to improve outcomes, which led to withdrawal of that particular indication; its skin-lymphoma role is the more settled one.
receptor fingerprint
Class I HDACs (via reduced thiol)inhibits (prodrug-activated)
Lymphoma cell apoptosisinduces
Safetyrisks and cautions, not medical advice
Romidepsin is an intravenous chemotherapy drug and is treated as a serious agent. Common problems include nausea and vomiting, fatigue, and bone-marrow suppression (low blood counts). Like other HDAC inhibitors it can affect the heart's electrical timing; trials watched for QT-interval changes and stressed keeping potassium and magnesium in the normal range, and it interacts with drugs that inhibit the CYP3A4 enzyme. It is administered by infusion under oncology supervision. There is no supplement or self-use context for this compound.
Interactionsdocumented pairs only, not exhaustive
Romidepsin is an intravenous histone deacetylase inhibitor, and its interactions matter because the therapeutic margin is narrow.
It is a substrate of both CYP3A4 and P-glycoprotein. Strong CYP3A inhibition raises exposure modestly; ketoconazole increased romidepsin AUC by about 25% in patients with advanced cancer. Rifampin behaved unexpectedly in the same programme, raising AUC by roughly 80% rather than lowering it, most likely by inhibiting hepatic uptake transporters, and thrombocytopenia was both more frequent and more severe as a result. Strong CYP3A inducers are therefore avoided outright rather than dose-adjusted. P-glycoprotein inhibitors such as quinidine and dronedarone also raise romidepsin levels.
Romidepsin prolongs the QT interval, so pairing it with other QT-prolonging agents, or giving it against a background of hypokalemia or hypomagnesemia, increases arrhythmia risk.
Prolonged prothrombin time and a raised INR have been reported when romidepsin was given alongside warfarin.
Checking a whole stack? Run it through interactions + stacks.
Subjective profileweighing the evidence above
A real oncology drug with durable responses in cutaneous T-cell lymphoma and unusually clever chemistry behind it. It is also an infusion given under specialist supervision, with nausea, low blood counts and cardiac timing to watch. There is no self-use context for it whatsoever.
Resources
This entry is here for reference.
Research
- 2012first citedRomidepsin: a histone deacetylase inhibitor for refractory cutaneous T-cell lymphoma
- 2023most recentRecent histone deacetylase inhibitors in cancer therapy
- 1.Histone Deacetylase Inhibitors for Cutaneous T-Cell Lymphoma
- 2.Targeting histone deacetylases in T-cell lymphoma
- 3.Recent histone deacetylase inhibitors in cancer therapy
- 4.Romidepsin for peripheral T-cell lymphoma
- 5.Romidepsin: a histone deacetylase inhibitor for refractory cutaneous T-cell lymphoma
5 listed here; entry last updated July 2026
Reviews
My notesprivate to this device
FAQ
Why is it called a prodrug?
It enters cells inactive, held closed by an internal disulfide bond. The reducing environment inside the cell breaks that bond and exposes a sulfur arm that then blocks the HDAC enzyme. So it only 'switches on' once it is inside.
What is a depsipeptide?
A ring-shaped molecule built from amino acids like a peptide but with at least one ester bond in place of a normal peptide bond. Romidepsin comes from a soil bacterium and has this unusual structure.
What is it approved for?
Cutaneous T-cell lymphoma (a skin lymphoma), and previously peripheral T-cell lymphoma. The peripheral indication was pulled back after a combination trial with chemotherapy failed to improve results.
Does it affect the heart?
It can influence the heart's electrical timing (QT interval), so clinicians keep potassium and magnesium in range and monitor patients; it is given by infusion in a supervised setting.
Adverse effects
- Nausea and vomiting
- Fatigue
- Low blood counts
- QT-interval / cardiac effects