Fenretinide

Synthetic retinoid agonist CAS# 65646-68-6

Fenretinide

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Chemical structure

Fenretinide

3D structure

Chemical Properties of Fenretinide

Cas No. 65646-68-6 SDF Download SDF
PubChem ID 5288209 Appearance Powder
Formula C26H33NO2 M.Wt 391.55
Type of Compound N/A Storage Desiccate at -20°C
Synonyms 4-HPR
Solubility Soluble to 100 mM in ethanol and to 100 mM in DMSO
Chemical Name (2E,4E,6E,8E)-N-(4-hydroxyphenyl)-3,7-dimethyl-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraenamide
SMILES CC1=C(C(CCC1)(C)C)C=CC(=CC=CC(=CC(=O)NC2=CC=C(C=C2)O)C)C
Standard InChIKey AKJHMTWEGVYYSE-FXILSDISSA-N
Standard InChI InChI=1S/C26H33NO2/c1-19(11-16-24-21(3)10-7-17-26(24,4)5)8-6-9-20(2)18-25(29)27-22-12-14-23(28)15-13-22/h6,8-9,11-16,18,28H,7,10,17H2,1-5H3,(H,27,29)/b9-6+,16-11+,19-8+,20-18+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Fenretinide

DescriptionSynthetic retinoid agonist. Antiproliferative, antioxidant and anticancer agent with a long half-life in vivo. Apoptotic effects appear to be mediated by a mechanism distinct from that of 'classical' retinoids.

Fenretinide Dilution Calculator

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Preparing Stock Solutions of Fenretinide

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.554 mL 12.7698 mL 25.5395 mL 51.079 mL 63.8488 mL
5 mM 0.5108 mL 2.554 mL 5.1079 mL 10.2158 mL 12.7698 mL
10 mM 0.2554 mL 1.277 mL 2.554 mL 5.1079 mL 6.3849 mL
50 mM 0.0511 mL 0.2554 mL 0.5108 mL 1.0216 mL 1.277 mL
100 mM 0.0255 mL 0.1277 mL 0.2554 mL 0.5108 mL 0.6385 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Fenretinide

Fenretinide(4HPR) is an inhibitor of Focal adhesion kinase (FAK) [1].

Fenretinideis a vitamin A analogue, it has been shown toinhibit the growth of many tumor cells, including small-cell lung cancer, malignant hemopoietic cells, and breast cancer cells. Fenretinide may also protectwomen against the development of ovarian cancer. The effect of Fenretinide on several gynecologic cancer cell lines shows the IC50 values of Fenretinide are only 0.3 and 0.4μM in two ovarian cancer cell lines(222and UCI 101) and are from 1 to 10μM in other ovarian cancer cell lines and cervical, endometrial cancer cell lines [2].

Fenretinide has also been shown to induce apoptosis inhuman prostate carcinoma cells (HPC).The IC50s of Fenretinide in LNCaP, DU145, and PC-3 are 0.9±0.16μM, 4.4±0.45μM and 3.0±1.0μM,respectively.Fenretinide induces this apoptosis through increasingROS and increasing enzymatic labeling of DNA breaks and formation of a DNA ladder. It is also reported that Fenretinide can impair prostate cancer cell migration and invasion by interfering with FAK/AKT/GSK3β pathway and β-catenin stability [1, 3].

References:
[1] Roberto Benelli, Stefano Monteghirfo, Roberta Venè, Francesca Tosettiand Nicoletta Ferrari.The chemopreventive retinoid 4HPR impairs prostate cancer cell migration and invasion by interfering with FAK/AKT/GSK3β pathway andβ-catenin stability. Molecular Cancer.2010, 9:142-154.
[2] Anita L. Sabichi, Denver T. Hendricks, Mary A. Bober, Michael J. Birrer. Retinoic acid receptorβexpression and growthinhibition of gynecologic cancer cells by thesynthetic retinoidn-(4-hydroxyphenyl) retinamide. Journal of the National Cancer Institute. 1998, 90(8): 597-605.
[3] Shi-Yong Sun, Ping Yue, and Reuben Lotan. Induction of apoptosis by n-(4-hydroxyphenyl)retinamide andits association with reactive oxygen species, nuclearretinoic acid receptors, and apoptosis-related genes in human prostate carcinoma cells.Molecular Pharmacology. 1999, 55:403–410.

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References on Fenretinide

Synthesis of short retinoidal amides related to fenretinide: antioxidant activities and differentiation-inducing ability.[Pubmed:28275870]

Cancer Chemother Pharmacol. 2017 Apr;79(4):725-736.

PURPOSE: By a scaffold shortening strategy, a small series of retinoidal amides Fenretinide (4-HPR) analogs have been synthesized from alpha, beta-ionones and tested for their antiproliferative and differentiating activities, and antioxidant effect. METHODS: The antiproliferative activity and triggering of apoptosis of our short retinoids were evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 4'-6-diamidino-2-phenylindole staining and microscope evaluation after 3- or 6-day exposure, while their differentiating activity was established by the analysis of the expression of the CD11b marker of differentiation in treated HL60 target cells and by the superoxide production assayed colorimetrically by the nitro blue tetrazolium-reducing activity assay. Finally, the antioxidant activity was determined by the 2,2'-azino-bis-(3-ethylbenzthiazoline-6-sulphonic acid) diammonium salt radical cation decolourisation assay utilizing the antioxidant Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid) as reference (Trolox equivalent antioxidant capacity, or TEAC). Docking analysis was performed to study the binding features to the Retinoic Acid Receptor alpha (RARalpha). RESULTS: While no pharmacologically relevant antiproliferative activity was evidenced, some of our short retinoids showed a differentiating and antioxidant activity similar to that of 4-HPR. In particular, compound 2b6 displayed a scavenging activity two times more efficient than 4-HPR itself. Finally, the docking analysis showed that these short retinoids, like 4-HPR, bind to the RARalpha protein with good fitness scores. CONCLUSION: Our data could pave the way for the design of new potent and less toxic antioxidant and differentiating compounds related to 4-HPR.

P450 inhibitor ketoconazole increased the intratumor drug levels and antitumor activity of fenretinide in human neuroblastoma xenograft models.[Pubmed:28340497]

Int J Cancer. 2017 Jul 15;141(2):405-413.

We previously reported that concurrent ketoconazole, an oral anti-fungal agent and P450 enzyme inhibitor, increased plasma levels of the cytotoxic retinoid, Fenretinide (4-HPR) in mice. We have now determined the effects of concurrent ketoconazole on 4-HPR cytotoxic dose-response in four neuroblastoma (NB) cell lines in vitro and on 4-HPR activity against two cell line-derived, subcutaneous NB xenografts (CDX) and three patient-derived NB xenografts (PDX). Cytotoxicity in vitro was assessed by DIMSCAN assay. Xenografted animals were treated with 4-HPR/LXS (240 mg/kg/day) + ketoconazole (38 mg/kg/day) in divided oral doses in cycles of five continuous days a week. In one model, intratumoral levels of 4-HPR and metabolites were assessed by HPLC assay, and in two models intratumoral apoptosis was assessed by TUNEL assay, on Day 5 of the first cycle. Antitumor activity was assessed by Kaplan-Meier event-free survival (EFS). The in vitro cytotoxicity of 4-HPR was not affected by ketoconazole (p >/= 0.06). Ketoconazole increased intratumoral levels of 4-HPR (p = 0.02), of the active 4-oxo-4-HPR metabolite (p = 0.04), and intratumoral apoptosis (p Fenretinide in neuroblastoma.

Fumonisin B1 Inhibits Endoplasmic Reticulum Stress Associated-apoptosis After FoscanPDT Combined with C6-Pyridinium Ceramide or Fenretinide.[Pubmed:28179290]

Anticancer Res. 2017 Feb;37(2):455-463.

BACKGROUND/AIM: Combining an anticancer agent Fenretinide (HPR) or C6-pyridinium ceramide (LCL29) with Foscan-mediated photodynamic therapy (FoscanPDT) is expected to augment anticancer benefits of each substance. We showed that treatment with FoscanPDT+HPR enhanced accumulation of C16-dihydroceramide, and that fumonisin B1 (FB), an inhibitor of ceramide synthase, counteracted caspase-3 activation and colony-forming ability of head and neck squamous cell carcinoma (HNSCC) cells. Because cancer cells appear to be more susceptible to increased levels of the endoplasmic reticulum (ER) stress than normal cells, herein we tested the hypothesis that FoscanPDT combined with HPR or LCL29 induces FB-sensitive ER stress-associated apoptosis that affects cell survival. MATERIALS AND METHODS: Using an HNSCC cell line, we determined: cell survival by clonogenic assay, caspase-3 activity by spectrofluorometry, the expression of the ER markers BiP and CHOP by quantitative real-time polymerase chain reaction and western immunoblotting, and sphingolipid levels by mass spectrometry. RESULTS: Similar to HPR+FoscanPDT, LCL29+FoscanPDT induced enhanced loss of clonogenicity and caspase-3 activation, that were both inhibited by FB. Our additional pharmacological evidence showed that the enhanced loss of clonogenicity after the combined treatments was singlet oxygen-, ER stress- and apoptosis-dependent. The combined treatments induced enhanced, FB-sensitive, up-regulation of BiP and CHOP, as well as enhanced accumulation of sphingolipids. CONCLUSION: Our data suggest that enhanced clonogenic cell killing after the combined treatments is dependent on oxidative- and ER-stress, apoptosis, and FB-sensitive sphingolipid production, and should help develop more effective mechanism-based therapeutic strategies.

Elevated Fibroblast growth factor 21 (FGF21) in obese, insulin resistant states is normalised by the synthetic retinoid Fenretinide in mice.[Pubmed:28256636]

Sci Rep. 2017 Mar 3;7:43782.

Fibroblast growth factor 21 (FGF21) has emerged as an important beneficial regulator of glucose and lipid homeostasis but its levels are also abnormally increased in insulin-resistant states in rodents and humans. The synthetic retinoid Fenretinide inhibits obesity and improves glucose homeostasis in mice and has pleotropic effects on cellular pathways. To identify Fenretinide target genes, we performed unbiased RNA-seq analysis in liver from mice fed high-fat diet +/- Fenretinide. Strikingly, Fgf21 was the most downregulated hepatic gene. Fenretinide normalised elevated levels of FGF21 in both high-fat diet-induced obese mice and in genetically obese-diabetic Lepr(db)mice. Moreover, Fenretinide-mediated suppression of FGF21 was independent of body weight loss or improved hepatic insulin sensitivity and importantly does not induce unhealthy metabolic complications. In mice which have substantially decreased endogenous retinoic acid biosynthesis, Fgf21 expression was increased, whereas acute pharmacological retinoid treatment decreased FGF21 levels. The repression of FGF21 levels by Fenretinide occurs by reduced binding of RARalpha and Pol-II at the Fgf21 promoter. We therefore establish Fgf21 as a novel gene target of Fenretinide signalling via a retinoid-dependent mechanism. These results may be of nutritional and therapeutic importance for the treatment of obesity and type-2 diabetes.

Pharmacokinetics of all-trans retinoic acid, 13-cis retinoic acid, and fenretinide in plasma and brain of Rat.[Pubmed:10640519]

Drug Metab Dispos. 2000 Feb;28(2):205-8.

We have measured the pharmacokinetics of three retinoids, all-trans retinoic acid, 13-cis retinoic acid, and Fenretinide in rat blood and rat brain [especially white matter (WM) and gray matter (GM)] to help select retinoids for treating human malignant glioma. All-trans retinoic acid permeated well into the WM, giving peak concentration in WM of 25.7 microg/g, 6 to 7 times higher than the peak serum concentration. There was less 13-cis retinoic acid in WM: area under the curve (AUC)(0-->infinity) WM/AUC(0-->infinity) serum = 18.00 microg ml(-1) h/32.67 microg ml(-1) h. The ratio WM/GM was over 1 for these two compounds, but the half-lives were short in the serum and cerebral tissue (0.57-1.02 h). Fenretinide had different pharmacokinetics: the peak concentrations were in serum (1.7 microg/ml) and WM (1.2 microg/ml)-low, but the AUC(0-->infinity) was large (25.55 microg ml(-1) in serum and 57.53 microg ml(-1) in WM) due to its long elimination half-life (13.78 h in serum and 17.77 h in WM). These findings provide information that may be used to select a retinoid and establish therapeutic regimens that provide optimal efficacy with minimal toxicity.

Antioxidant properties of N-(4-hydroxyphenyl)retinamide (fenretinide).[Pubmed:10706389]

Biol Pharm Bull. 2000 Feb;23(2):222-5.

Fenretinide, N-(4-hydroxyphenyl)retinamide (4-HPR), is a cancer chemopreventive and antiproliferative agent whose mechanism of action is unknown. 4-HPR is a potent inducer of apoptosis in HL60 human leukemia cells which generates intracellular reactive oxygen species. The structural similarity of retinoic acid (RA), 4-HPR, and alpha-tocopherol (vitamin E) led us to investigate whether 4-HPR exhibits antioxidant activity. It was found that 4-HPR scavenged alpha,alpha-diphenyl-beta-picrylhydrazyl (DPPH) radicals in a 1:1 ratio in contrast to vitamin E, where a 1:2 ratio relative to DPPH radicals was observed. In addition, linoleic acid peroxidation initiated by hydroxyl radicals was decreased by 4-HPR to the same extent as by vitamin E. Furthermore, lipid peroxidation in rat liver microsomes was reduced by 4-HPR to a greater extent than by vitamin E. Based on these results, 4-HPR appears to be an effective antioxidant that may have clinical utility for diseases treated with vitamin E.

Fenretinide and its relation to cancer.[Pubmed:10448131]

Cancer Treat Rev. 1999 Aug;25(4):229-35.

Retinoids, natural or synthetic substances which have vitamin A activity, have a well-known reputation for their antitumour and differention-inducing activity in vitro and in vivo. More than 1500 retinoids have been tested so far but very few of them have been entered into clinical trials because of their side-effects. All-trans-N-(4-hydroxyphenyl)retinamide (4HPR or Fenretinide) is a synthetic retinoid that is reported to have fewer side-effects compared to naturally occurring retinoids such as all-trans retinoic acid (ATRA) and 9-cis retinoic acid. In addition, Fenretinide has been shown to induce cell death (apoptosis) even in ATRA-resistant cell lines. Although the mechanism by which Fenretinide acts is not entirely known it is considered to be a promising drug and seems to induce apoptosis via different pathway(s) from classical retinoids. In this review, we discuss possible mechanisms of Fenretinide action and summarize results of clinical trials.

Description

Synthetic retinoid; antiproliferative and antioxidant,Tretinoin, which is a ligand for both the retinoic acid receptor (RAR) and the retinoid X receptor (RXR), can induce granulocytic differentiation and apoptosis in acute promyelocytic leukemia (APL) cells.

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