Evidence Grade A — Regulatory approved. 809 published studies. 105 registered clinical trials.
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Romidepsin (sold as Istodax) is an intravenous cancer treatment for rare forms of T-cell lymphoma — cancers of a specific type of white blood cell. Derived from a soil bacterium, it enters cancer cells in disguise and then switches on genes that the cancer had silenced to avoid self-destruction. It is one of very few effective treatments available for these rare lymphomas.
Romidepsin is also known by these brand and alternate names:
809 published studies: 630 human, 35 animal, 212 in-vitro, 164 reviews
Romidepsin is marketed as Istodax (approved November 2009 for cutaneous T-cell lymphoma; June 2011 for peripheral T-cell lymphoma). Administered as an intravenous infusion over 4 hours on a cyclical schedule.
In T-cell lymphoma trials, romidepsin achieved response rates of 25–34%, with some durable complete responses lasting over two years. A Phase III trial (Ro-CHOP) adding romidepsin to standard chemotherapy for peripheral T-cell lymphoma did not meet its primary endpoint, which has narrowed its role primarily to relapsed disease. The main side effects include nausea, fatigue, low blood counts, and ECG changes. Romidepsin occupies a niche in a disease area with very few effective treatments.
Cancer cells often survive by chemically silencing tumour suppressor genes — the genes that would normally tell a damaged cell to stop dividing or self-destruct. They do this by keeping DNA tightly wound around proteins called histones. Romidepsin enters the cell in a disguised, inactive form. Once inside, the cell's own chemistry activates it, releasing zinc-binding arms that block the enzymes (HDACs) responsible for keeping DNA wound tight. This loosens the DNA, reactivating the silenced tumour suppressor genes and triggering cancer cell death.
In T-cell lymphoma trials, romidepsin achieved response rates of 25–34%, with some patients experiencing durable complete responses lasting over two years. For a cancer type with very few effective treatments, these response rates are clinically meaningful — though the majority of patients did not respond. A Phase III trial (Ro-CHOP) testing romidepsin as part of frontline combination chemotherapy did not meet its primary endpoint, which has narrowed its role primarily to relapsed or refractory disease. Side effects include nausea, fatigue, low blood counts, and ECG changes requiring cardiac monitoring. The drug's mechanism — reactivating silenced tumour-suppressor genes by loosening how DNA is packaged — represents an important concept in cancer biology that continues to be explored in combination with newer immunotherapy approaches.
PeptideTrace tracks 105 registered clinical trials for Romidepsin sourced from ClinicalTrials.gov.
A Multicenter, Open-Label Continuation Trial Evaluating the Tolerability and Activity of Depsipeptide (FK228) in Patients That Have Completed a Prior Clinical Study With Depsipeptide.
Study Investigating Intravesical HDAC Inhibition to Improve Response to Immuno-Oncology Agents
Evaluation of the Safety and the Tolerability of a Combination of Two HIV Inducers in Patients With Undetectable Viral Load
Doxorubicin, CC-(486) (5-azacitidine), Romidepsin, and Duvelisib (hARD) for T-cell Lymphoma
Romidepsin and Parsaclisib for the Treatment of Relapsed or Refractory T-Cell Lymphomas
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Health Canada Market Authorisation
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FDA ORIG 1
Romidepsin (FK228) is a bicyclic depsipeptide from Chromobacterium violaceum, MW 540.71 Da. Depsipeptide macrocycle (4 AA + ester bond) bridged by disulfide bond. Natural prodrug: intracellular glutathione reduces disulfide to release zinc-binding thiols. IV 14 mg/m2 over 4h on Days 1, 8, 15 of 28-day cycle. Half-life ~3 hours.
Prodrug activated intracellularly by glutathione reduction of disulfide bridge, generating free thiols that chelate Zn2+ in Class I HDAC catalytic pocket (HDAC1/2/3/8, IC50 1-10 nM). Increases histone acetylation, reactivating silenced tumor suppressors (p21, CDKN1A). Also induces apoptosis, cell cycle arrest, angiogenesis inhibition, and MHC I/NKG2D upregulation.
Marketed as Istodax. Approved November 5, 2009 (CTCL) and June 18, 2011 (PTCL). CTCL pivotal (N=96): ORR 34% (6% CR), median DOR 15.0 months. PTCL pivotal (N=130): ORR 25% (15% CR/CRu), DOR 28 months. Ro-CHOP Phase III (N=421) did not meet PFS endpoint (12.0 vs. 10.2 months, P=0.096). Indications: relapsed CTCL and PTCL after >=1 prior therapy.
Vancomycin is marketed as Vancocin and Firvanq (approved 1958, with oral solution Firvanq approved 2018). It is the standard treatment for serious MRSA infections (bloodstream infections, endocarditis, pneumonia, bone infections) and is first-line for severe C. difficile colitis. Vancomycin requires therapeutic drug monitoring — blood levels must be checked regularly to ensure the dose is effective without causing kidney damage or hearing loss. The rise of vancomycin-resistant enterococci (VRE) and occasional vancomycin-intermediate S. aureus (VISA) strains represent ongoing challenges. Despite being nearly 70 years old, vancomycin remains irreplaceable for many serious infections, though newer alternatives like daptomycin and the lipoglycopeptides offer advantages in specific settings.
Zilucoplan is marketed as Zilbrysq (approved October 2023) for anti-acetylcholine receptor antibody-positive generalised myasthenia gravis in adults. Administered as a daily subcutaneous self-injection. In the RAISE trial, zilucoplan showed statistically significant improvements in both activities of daily living and quantitative muscle strength scores compared to placebo, with improvements evident from week one. Its key differentiator from existing complement inhibitors (eculizumab, ravulizumab) is the self-injectable format — those alternatives require hospital-based intravenous infusions. As with all complement inhibitors, patients require meningococcal vaccination before starting treatment due to increased susceptibility to meningococcal infection.
Daptomycin is marketed as Cubicin (approved September 2003). It is indicated for complicated skin and soft tissue infections and S. aureus bloodstream infections including right-sided endocarditis. Administered as a once-daily intravenous infusion. A key limitation is that daptomycin cannot be used for pneumonia — lung surfactant inactivates the drug. In the bacteraemia trial, daptomycin was non-inferior to vancomycin with significantly lower rates of kidney problems (11% versus 26%). Creatine kinase (CK) levels must be monitored during treatment, as daptomycin can cause muscle toxicity. Generics became available after patent expiry, significantly reducing cost.
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