Inhibition of Aldo-Keto Reductase (AKR)

General Discussion
#1

@Axolotl, a question: the inhibition of Aldo-Keto Reductase (AKR), can lead to PFS?


The substance I take, Oxerutin, inhibits shit. Could I have developed it from here?

http://clincancerres.aacrjournals.org/content/19/20/5613

Aldo-keto reductase family 1 member C3 https://www.uniprot.org/uniprot/P42330

Catalyzes the conversion of aldehydes and ketones to alcohols. Catalyzes the reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ) and the oxidation of 9-alpha,11-beta-PGF2 to PGD2. Functions as a bi-directional 3-alpha-, 17-beta- and 20-alpha HSD. Can interconvert active androgens, estrogens and progestins with their cognate inactive metabolites. Preferentially transforms androstenedione (4-dione) to testosterone.

Strongly inhibited by nonsteroidal anti-inflammatory drugs (NSAID) including flufenamic acid and indomethacin. Also inhibited by the flavinoid, rutin, and by selective serotonin inhibitors (SSRIs).

I’m still trying to understand why a success, there are no cases I’m the only one to have the PFS from Oxerutina!

I discovered things, but I would like to confirm.

Omar

#2

https://www.researchgate.net/publication/26282042_Inhibition_of_Human_Steroid_5_-Reductase_AKR1D1_by_Finasteride_and_Structure_of_the_Enzyme-Inhibitor_Complex
Oh fuck! :worried::worried::worried:

#3

@axolotl Could this enzyme be the cause of my problem?

#4

It could cause problems with DHT catabolism.

#5

In order to further investigate the link of AKR1C1/1C2 expression with inflammation and drug resistance, H23 cells, which exhibited low baseline AKR1C1/1C2 expression and higher drug sensitivity (Fig. 1 a and Table II), were chosen for the following experiments. Firstly, to assess the effects of pro‐inflammatory factors on AKR1C1/1C2 expression, H23 cells were treated with 5 ng/ml of IL‐6, 5 mM of n ‐sodium butyrate ( n ‐BT), 25 ng/ml of phorbol myristate acetate (PMA), or 30 ng/ml of platelet activating factor (PAF) respectively. In 24 hr, immunoblots showed clearly upregulated AKR1C1/1C2 expression in H23 cells

https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.22402

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