Finasteride-d9 is intended for use as an internal standard for the quantification of finasteride (Item No. 14938) by GC- or LC-MS. Finasteride is a 4-azasteroid competitive inhibitor of 5α-reductase type II (IC50 = 4.2 nM) and a derivative of testosterone.{23862} It is 100-fold selective for 5α-reductase type II over type I. Finasteride (10 µM) does not affect the growth of androgen-refractory PC3 prostate cancer cells but increases the protein levels of Nrf2 and heme oxygenase-1 (HO-1).{23866} It decreases prostatic diameter and volume, as well as dihydrotestosterone, but not testosterone, serum levels in dogs with spontaneous benign prostatic hypertrophy when administered at doses of 0.1 and 0.5 mg/kg.{48477} Finasteride reduces testosterone-induced type I procollagen and TGF-β1 protein levels in cultured human scalp dermal fibroblasts in a model of androgenic alopecia when applied at a concentration of 0.1 μM.{23865} Formulations containing finasteride have been used in the treatment of benign prostatic hyperplasia and androgenic alopecia in men.
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An internal standard for the quantification of finasteride by GC- or LC-MS
Formal name: (4aR,4bS,6aS,7S,9aS,9bS,11aR)-4a,6a-dimethyl-N-(2-(methyl-d3)propan-2-yl-1,1,1,3,3,3-d6)-2-oxo-2,4a,4b,5,6,6a,7,8,9,9a,9b,10,11,11a-tetradecahydro-1H-indeno[5,4-f]quinoline-7-carboxamide
Synonyms:
Molecular weight: 381.6
CAS: 1131342-85-2
Purity: ≥99% deuterated forms (d1-d9)
Formulation: A solid
Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression and are therefore promising targets for cancer therapy. (R)-Roscovitine is a potent inhibitor of Cdk2/cyclin E with an IC50 value of 0.1 µM.{14988} It also inhibits Cdk7/cyclin H, Cdk5/p35, and cell division cycle (cdc)/cyclin B with IC50 values of 0.49, 0.16, and 0.65 µM, respectively.{14987,14988,14991} (R)-Roscovitine inhibits the growth of rapidly proliferating cells with an average IC50 value of 15.2 µM against a panel of 19 human tumor cell lines.{14988} In murine models of polycystic kidney disease, (R)-roscovitine effectively inhibited disease progression at doses of 50-100 mg/kg.{14564}
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The tetracycline repressor (TetR) is a transcriptional regulator which normally binds tightly to its palindromic tetO operator DNA, blocking gene expression.{17508} Tet causes the repressor to dissociate from the DNA, allowing transcription to occur. A novel reverse TetR (revTetR) requires tetracycline as a co-repressor to bind tetO and block transcription.{17509,17510} Anhydrotetracycline (hydrochloride) is a powerful effector in both the tetracycline repressor (TetR) and reverse TetR (revTetR) systems, binding the Tet repressor 35-fold more strongly than Tet.{17508,17511} Moreover, anhydrotetracycline poorly binds the 30S ribosomal subunit, compared to Tet,{17512} so it does not act as a general inhibitor of translation and is a poor antibiotic. Perhaps related to this, the concentration of anhydrotetracycline that inhibits eukaryotic cell growth is more than a 1,000-fold above the dose that alters transcription through TetR.{17508}
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Cyclin-dependent kinases (CDKs) are key regulators of cell cycle progression and are therefore promising targets for cancer therapy. (R)-Roscovitine is a potent inhibitor of Cdk2/cyclin E with an IC50 value of 0.1 µM.{14988} It also inhibits Cdk7/cyclin H, Cdk5/p35, and cell division cycle (cdc)/cyclin B with IC50 values of 0.49, 0.16, and 0.65 µM, respectively.{14987,14988,14991} (R)-Roscovitine inhibits the growth of rapidly proliferating cells with an average IC50 value of 15.2 µM against a panel of 19 human tumor cell lines.{14988} In murine models of polycystic kidney disease, (R)-roscovitine effectively inhibited disease progression at doses of 50-100 mg/kg.{14564}
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The maintenance of embryonic stem cells in culture typically requires feeder cells and various exogenous factors found in serum. Murine embryonic stem (mES) cells can be maintained in the absence of feeder cells and serum but require the leukemia inhibitor factor (LIF) and bone morphogenic protein (BMP) to prevent differentiation and promote self-renewal. SC-1 is a small molecule activator of stem cell renewal that allows the propagation of OG2 mES cells for at least 10 passages in an undifferentiated state.{14533} The activity of SC-1 is mediated by the combined inhibition of RasGAP and ERK1 with Kd values of 98 and 212 nM, respectively.{14533} Inhibition of RasGAP increases Ras signaling via the PI3-kinase pathway which promotes self-renewal, whereas inhibition of ERK blocks differentiation.
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