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Forskolin
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Product Name Forskolin
Price: $40 / 20mg
CAS No.: 66575-29-9
Catalog No.: CFN90186
Molecular Formula: C22H34O7
Molecular Weight: 410.50 g/mol
Purity: >=98%
Type of Compound: Diterpenoids
Physical Desc.: White powder
Source: The herbs of Coleus forskohlii
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF
Similar structural: Comparison (Web)  (SDF)
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Size /Price /Stock 10 mM * 1 mL in DMSO / $12.7 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Forskolin is a ubiquitous activator of eukaryotic adenylyl cyclase (AC) in a wide variety of cell types, commonly used to raise levels of cAMP in the study and research of cell physiology. Forskolin has antitumor, antioxidant and antiinflammatory actions, it may cause genotoxic effects. Chronic administration of Forskolin can decrease fasting blood glucose levels, it is effective in preventing diet induced obesity.
Targets: cAMP | Akt | ERK | Adenylyl cyclase | cGMP | FFA | PP2A | Caspase
In vitro:
Mutat Res Genet Toxicol Environ Mutagen. 2015 Jan 1;777:29-32.
Forskolin: genotoxicity assessment in Allium cepa.[Pubmed: 25726172]
Forskolin, a diterpene, 7β-acetoxy-8,13-epoxy-1α,6β,9α-trihydroxy-labd-14-en-11-one (C22H34O7) isolated from Coleus forskohlii, exerts multiple physiological effects by stimulating the enzyme adenylate cyclase and increasing cyclic adenosine monophosphate (cAMP) concentrations. Forskolin is used in the treatment of hypertension, congestive heart failure, eczema, and other diseases.
METHODS AND RESULTS:
A cytogenetic assay was performed in Allium cepa to assess possible genotoxic effects of Forskolin. Forskolin was tested at concentrations 5-100 μM for exposure periods of 24 or 48 h. Treated samples showed significant reductions in mitotic index (p < 0.05) and increases in the frequency of chromosome aberrations (p < 0.01) at both exposure times. The treated meristems showed chromosome aberrations including sticky metaphases, sticky anaphases, laggard, anaphase bridges, micronuclei, polyploidy, fragments, breaks, and C-mitosis.
CONCLUSIONS:
Forskolin may cause genotoxic effects and further toxicological evaluations should be conducted to ensure its safety.
J Reprod Dev. 2014 Mar 7;60(1):78-82.
Effect of leukemia inhibitory factor and forskolin on establishment of rat embryonic stem cell lines.[Pubmed: 24317016]
This study was designed to investigate whether supplementation of 2i medium with leukemia inhibitory factor (LIF) and/or Forskolin would support establishment of germline-competent rat embryonic stem (ES) cell lines.
METHODS AND RESULTS:
Due to the higher likelihood of outgrowth rates, supplementation of Forskolin with or without LIF contributed to the higher establishment efficiency of ES cell lines in the WDB strain. Germline transmission competency of the chimeric rats was not influenced by the profile of ES cell lines until their establishment. When the LIF/Forskolin-supplemented 2i medium was used, the rat strain used as the blastocyst donor, such as the WI strain, was a possible factor negatively influencing the establishment efficiency of ES cell lines. Once ES cell lines were established, all lines were found to be germline-competent by a progeny test in chimeric rats.
CONCLUSIONS:
In conclusion, both LIF and Forskolin are not essential but can play a beneficial role in the establishment of "genuine" rat ES cell lines.
Sci Rep . 2018 May 25;8(1):8161.
High-throughput screening identified selective inhibitors of exosome biogenesis and secretion: A drug repurposing strategy for advanced cancer[Pubmed: 29802284]
Abstract Targeting exosome biogenesis and release may have potential clinical implications for cancer therapy. Herein, we have optimized a quantitative high throughput screen (qHTS) assay to identify compounds that modulate exosome biogenesis and/or release by aggressive prostate cancer (PCa) CD63-GFP-expressing C4-2B cells. A total of 4,580 compounds were screened from the LOPAC library (a collection of 1,280 pharmacologically active compounds) and the NPC library (NCGC collection of 3,300 compounds approved for clinical use). Twenty-two compounds were found to be either potent activators or inhibitors of intracellular GFP signal in the CD63-GFP-expressing C4-2B cells. The activity of lead compounds in modulating the secretion of exosomes was validated by a tunable resistive pulse sensing (TRPS) system (qNano-IZON) and flow cytometry. The mechanism of action of the lead compounds in modulating exosome biogenesis and/or secretion were delineated by immunoblot analysis of protein markers of the endosomal sorting complex required for transport (ESCRT)-dependent and ESCRT-independent pathways. The lead compounds tipifarnib, neticonazole, climbazole, ketoconazole, and triademenol were validated as potent inhibitors and sitafloxacin, Forskolin, SB218795, fenoterol, nitrefazole and pentetrazol as activators of exosome biogenesis and/or secretion in PC cells. Our findings implicate the potential utility of drug-repurposing as novel adjunct therapeutic strategies in advanced cancer.
In vivo:
Biotech Histochem. 2014 Jul;89(5):388-92.
The effects of forskolin and rolipram on cAMP, cGMP and free fatty acid levels in diet induced obesity.[Pubmed: 24520882]
Obesity is a major health problem. We investigated the effects of Forskolin and rolipram in the diet of animals in which obesity had been induced.
METHODS AND RESULTS:
We used 50 female albino Wistar rats that were assigned randomly into five groups as follows: group 1, control; group 2, high fat diet; group 3, high fat diet + Forskolin; group 4, high fat diet + rolipram; and group 5, high fat diet + rolipram + Forskolin. The rats were fed for 10 weeks and rolipram and Forskolin were administered during last two weeks. The animals were sacrificed and blood samples were obtained. Serum cAMP, cGMP and free fatty acids (FFA) levels were measured using ELISA assays. We also measured weight gain during the 10 week period. cAMP and FFA levels of groups 3, 4 and 5 were significantly higher than those of groups 1 and 2. We found no significant differences in serum cGMP levels among the groups. The weight gain in groups 3, 4 and 5 was significantly less than for group 2. We also found that the weight gain in group 5 was significantly less than in groups 3 and 4.
CONCLUSIONS:
We found that both Forskolin and rolipram stimulated lipolysis and inhibited body weight increase by increasing cAMP levels. Also, combination therapy using the two agents may be more effective in preventing diet induced obesity than either agent alone. We found also that these agents did not effect cellular cGMP levels in diet induced obesity.
Forskolin Description
Source: The herbs of Coleus forskohlii
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.4361 mL 12.1803 mL 24.3605 mL 48.7211 mL 60.9013 mL
5 mM 0.4872 mL 2.4361 mL 4.8721 mL 9.7442 mL 12.1803 mL
10 mM 0.2436 mL 1.218 mL 2.4361 mL 4.8721 mL 6.0901 mL
50 mM 0.0487 mL 0.2436 mL 0.4872 mL 0.9744 mL 1.218 mL
100 mM 0.0244 mL 0.1218 mL 0.2436 mL 0.4872 mL 0.609 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Biochim Biophys Acta. 2014 Sep;1842(9):1823-9.
Hyperphosphorylation of PP2A in colorectal cancer and the potential therapeutic value showed by its forskolin-induced dephosphorylation and activation.[Pubmed: 24997451]
The tumor suppressor protein phosphatase 2A (PP2A) is frequently inactivated in human cancer and phosphorylation of its catalytic subunit (p-PP2A-C) at tyrosine-307 (Y307) has been described to inhibit this phosphatase. However, its molecular and clinical relevance in colorectal cancer (CRC) remains unclear.
METHODS AND RESULTS:
p-PP2A-C Y307 was determined by immunoblotting in 7 CRC cell lines and 35 CRC patients. CRC cells were treated with the PP2A activator Forskolin alone or combined with the PP2A inhibitor okadaic acid, 5-fluorouracil and oxaliplatin. We examined cell growth, colonosphere formation, caspase activity and AKT and ERK activation. PP2A-C was found hyperphosphorylated in CRC cell lines. Forskolin dephosphorylated and activated PP2A, impairing proliferation and colonosphere formation, and inducing activation of caspase 3/7 and changes in AKT and ERK phosphorylation. Moreover, Forskolin showed additive effects with 5-fluorouracil and oxaliplatin treatments. Analysis of p-PP2A-C Y307 in primary tumors confirmed the presence of this alteration in a subgroup of CRC patients.
CONCLUSIONS:
Our data show that PP2A-C hyperphosphorylation is a frequent event that contributes to PP2A inhibition in CRC. Antitumoral effects of Forskolin-mediated PP2A activation suggest that the analysis of p-PP2A-C Y307 status could be used to identify a subgroup of patients who would benefit from treatments based on PP2A activators.
Animal Research:
Int J Med Sci. 2014 Mar 11;11(5):448-52.
Effect of chronic administration of forskolin on glycemia and oxidative stress in rats with and without experimental diabetes.[Pubmed: 24688307]
Forskolin is a diterpene derived from the plant Coleus forskohlii. Forskolin activates adenylate cyclase, which increases intracellular cAMP levels. The antioxidant and antiinflammatory action of Forskolin is due to inhibition of macrophage activation with a subsequent reduction in thromboxane B2 and superoxide levels. These characteristics have made Forskolin an effective medication for heart disease, hypertension, diabetes, and asthma.
METHODS AND RESULTS:
Here, we evaluated the effects of chronic Forskolin administration on blood glucose and oxidative stress in 19 male Wistar rats with streptozotocin-induced diabetes compared to 8 healthy male Wistar rats. Rats were treated with Forskolin, delivered daily for 8 weeks. Glucose was assessed by measuring fasting blood glucose in diabetic rats and with an oral glucose tolerance test (OGTT) in healthy rats. Oxidative stress was assessed by measuring 8-hydroxydeoxyguanosine (8‑OHdG) in 24-h urine samples. In diabetic rats, without Forskolin, fasting blood glucose was significantly higher at the end than at the beginning of the experiment (8 weeks). In both healthy and diabetic rats, Forskolin treatment lowered the fasting glucose at the end of the experiment but no effect was found on oral glucose tolerance. The 8-OHdG levels tended to be less elevated in Forskolin-treated than in untreated group.
CONCLUSIONS:
Our results showed that chronic administration of Forskolin decreased fasting blood glucose levels; however, the reductions of 8-OHdG were not statistically significant.
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