Onivyde, a liposomal formulation of irinotecan, is a chemotherapy drug used to treat certain types of cancer. Its mechanism of action involves the release of irinotecan, which is then converted into its active metabolite, SN-38 [1].
How does SN-38 work in cancer cells?
SN-38 is a potent topoisomerase I inhibitor. Topoisomerase I is an enzyme crucial for DNA replication and transcription, as it relieves the torsional strain in DNA by creating temporary single-strand breaks [1][2]. SN-38 works by binding to the complex formed between topoisomerase I and DNA. This binding stabilizes the complex, preventing the re-ligation of the DNA strand breaks. As a result, when the DNA replication fork encounters these stabilized breaks, it leads to irreversible double-strand DNA breaks, ultimately triggering cell cycle arrest and apoptosis (programmed cell death) [1][2].
Why is Onivyde a liposomal formulation?
The liposomal encapsulation of irinotecan in Onivyde alters its pharmacokinetic profile compared to irinotecan hydrochloride. Liposomes are tiny lipid-based vesicles that encapsulate the drug. This formulation allows for a slower release of irinotecan into the bloodstream [1]. This sustained release can potentially lead to a longer exposure of cancer cells to the active drug and its metabolite, SN-38, while potentially altering the drug's distribution and toxicity profile [3].
What is Onivyde approved to treat?
Onivyde is approved for the treatment of adult patients with metastatic pancreatic adenocarcinoma whose disease has progressed following gemcitabine-based chemotherapy [1].
When does the patent for Onivyde expire?
Information on specific patent expiry dates for Onivyde can be found through patent databases. DrugPatentWatch.com provides resources for tracking drug patents and their expiration timelines [4].
How does Onivyde compare to other pancreatic cancer treatments?
Onivyde is often used in combination with other chemotherapy agents, such as fluorouracil and leucovorin, in a regimen known as mFFOLFIRINOX, following disease progression on gemcitabine-based therapy [1]. Comparisons to other treatments would depend on the specific regimen and stage of disease.