repurposing: a newly published summary

[Maxone73]

with a useful list of current and recent trials…

nature.com/articles/s41392-...

[cujoe]

Darn fine find, Max. Thanks for posting. I've got a companion resource that I will try to get posted later tonight or over the weekend.

Be S&W - ciao cj

[rsgdmd in reply to cujoe]

I recently had functional testing done on bone biopsy sample. The SOC drug that worked best was mitoxantrone, which was the chemo used 20+ years ago before docetaxel came on the scene. Of the off label & repurposed drugs, disulfiram (Antabuse) showed the most activity.

[Maxone73 in reply to rsgdmd]

Where did you have it done? I have been thinking about Artemisinin lately, maybe I could try iy in a few months, even if it is surely not as bioavailable as its synthetic version.

[rsgdmd]

I had the bone biopsy done at Penn, where my MO is. I asked for it as I had arranged for functional testing thru Sage Medic and sequencing thru Boston Gene. They took cores that I took with me and FedEx'd to both companies. They also did path there, which showed adenocarcinoma - no surprise. Unfortunately, Boston Gene couldn't get enough cells to do sequencing.

[KocoPr]

i like the mechanism of action of

Disulfiram

Disulfiram (DSF), also known by its trade name Antabuse

For example, Du et al. found that DSF inhibited the glycolysis of cancer cells in a copper-dependent manner. Furthermore, a combination of DSF and copper was shown to significantly reduce the expression levels of key molecules, including S6K1, MYC, and their downstream targets, glucose transporter 1 (GLUT1), PKM2, and lactate dehydrogenase A (LDHA), which are integral to the regulation of critical cellular processes, such as apoptosis, cell differentiation, and metabolism.112

Oleanolic acid (OA)

OA has also emerged as an epigenetic modulator in immunotherapy for cancer. OA was shown to inhibit the IL-1/NF-κB/TET3 axis in cancer cells, resulting in DNA hypomethylation and the suppression of PD-L1, thereby strengthening the robust T-cell defense mechanism. In addition, synthetic derivatives of OA, such as CDDO-Im, have been shown to block the EGFR/signal transducer and activator of transcription 3 (STAT3)/Sox-2 signaling pathway in tumor-associated macrophages (TAMs), which have been implicated in promoting breast cancer proliferation and metastasis.

simvastatin is particularly interesting due to its anticancer applications, which have been observed in various cancer types and are largely mediated through activation of mutant P53. Specifically, simvastatin was found to reduce the migratory and invasive abilities of human epithelial MDA-MB-231 breast cancer cells in vitro by increasing mutant P53 expression and repressing expression of the stem cell marker CD44, which is essential for cell migration. Similarly, in MDA-MB231 mouse xenograft models, simvastatin treatment led to elevated P53 and reduced CD44 expression levels. Ongoing clinical trials are currently examining the efficacy of simvastatin against various cancers, including breast (NCT00807950, NCT05550415), gastric (NCT01099085, NCT03086291), colorectal (NCT01238094), and bladder (NCT02360618) cancer. Although the specifics of its mechanism, optimal dosage, and compatibility with other anticancer drugs remain unclear, we anticipate the emergence of novel strategies employing statins in cancer treatment in the future.

This article goes on and on with so many more drugs and phytonutrients like EGCG.

I have to get back to it later! Good reference to keep around!