Innovation Pharmaceuticals Inc (IPIX)

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Of course there is more if you have interest.

TP53 signal pathway confers potential therapy target in acute myeloid leukemia
First published: 24 January 2023
"Future research will be needed to address not only the underlying mechanism of the TP53-associated pathway in AML but the related selective pressures as well. Diverse drugs have the potential to treat tp53-mutated AML. As an example, triptolide could activate tumor suppressor p53.83 In addition, Kevetrin has been reported to be effective against primary wt- and mut-TP53 AML patients and has been found activity via p53-dependent and nondependent pathways in solid tumors. Although its functions in leukemic cells remain unknown, these findings suggest that Kevetrin will be a potential therapeutic strategy for TP53 mutant AML."
https://onlinelibrary.wiley.com/doi/10.1111/ejh.13934

Recent findings on the role of wild-type and mutant p53 in cancer development and therapy
Frontiers in Molecular Biosciences, 26 Sep 2022
"The kevetrin (thiobutyronitrile), which has an inhibitory effect on histone deacetylase (HDAC), can directly affect mutant p53 and lead to p53 phosphorylation in serine 15 and cessation of cell division in the G2/M stage and finally tumor cell death. It should be noted that its role in inhibiting ovarian cancer cell lines is well known (Kumar et al., 2011; Kumar et al., 2017)."
https://europepmc.org/article/pmc/pmc9549909

Semiconducting polymer nanomanipulators for thermal sensitization and metastasis-inhibited synergistic cancer therapy
Accepted 13 November 2022, Available online 21 November 2022, Version of Record 21 November 2022
"Manipulation of intracellular protein expression provides a novel therapeutic strategy for cancer therapy [1], [2], [3]. Delivery of molecular drugs into cancer cells to manipulate oncogenic or antioncogenic protein expression has been considered a promising cancer therapeutic approach [4], [5]. For example, hypoxia-inducible transcription factor (HIF)- 1a inhibitors, such as KC7F2 or YC-1, inhibit HIF-1a expression levels by promoting HIF-1a degradation and downregulating HIF-1a protein synthesis to achieve an effective antitumor effect [6], [7]. Kevetrin, a small molecular activator of the tumor suppressor protein p53, activates p53, which in turn upregulates the expression of p21 to induce cell cycle arrest and apoptosis [8]."
https://www.sciencedirect.com/science/article/abs/pii/S174801322200319X

Inhibition of mycobacteria proliferation in macrophages by low cisplatin concentration through phosphorylated p53-related apoptosis pathway
2023 Jan 31
"The results of Western blot detection showed that the expression of phosphorylated p53 protein increased after DDP treatment, and this effect was positively correlated with the concentration and the time of DDP treatment (Fig 4A and 4B). The CFU by spread plate method showed in DDP combined with p53 promoter (Kevetrin hydrochloride) group decreased significately compared with DDP group (p<0.0001), while the number of colonies in DDP combined with p53 inhibitor (Pifithrin -a hydrobromide) group increased greatly compared with DDP group (p<0.0001) (Fig 4C). Moreover, the bacterial number in cells could also be significantly reduced by using Kevetrin hydrochloride alone, and this effect was positively correlated with the concentration of the p53 promoter.
The p53 promoter Kevetrin hydrochloride scavenges intracellular mycobacteria. If combined with DDP, Kevetrin hydrochloride could increase the effect of DDP on the elimination of intracellular mycobacteria.
Conclusion: DDP may be a new host-directed therapy for tuberculosis treatment, as well as the p53 promoter Kevetrin hydrochloride."
https://pubmed.ncbi.nlm.nih.gov/36719870/