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Product name: Forskolin
Synonym name: Coleonol; Colforsin, Boforsin
Catalogue No.: BP0593
Cas No.: 66575-29-9
Formula: C22H34O7
Mol Weight: 410.507
Botanical Source: Coleus forskohlii
Physical Description:
Type of Compound: Diterpenoids
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever 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 -20℃. Generally, these will be useable for up to two weeks.
The product could be supplied from milligrams to grams
Inquire for bulk scale.
Description:
Oridonin has anticancer activity, might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.It inhibits tumor growth in glioma by inducing cell cycle arrest and apoptosis, inhibits BxPC-3 cell growth through cell apoptosis.
References:
Sichuan Da Xue Xue Bao Yi Xue Ban. 2014 Nov;45(6):903-7.
Anti-leukemia effect of oridonin on T-cell acute lymphoblastic leukemia
To investigate the antileukemia effect of Oridonin on T-cell acute lymphoblastic leukemia cell line CEM.
METHODS AND RESULTS:
Human T-cell acute lymphoblastic leukemia cell line CEM was cultured in vitro. The 50% inhibition concentration (IC50) of Oridonin against CEM cells was examined using modified MTT assay. The cellular morphologic changes were observed using a light microscope. The percent of apoptosis of CEM cells after drug treatment was evaluated by flow cytometric analysis. The active levels of AKT/mTOR, RAF/MEK/ ERK, STAT5 signaling pathways and the expression levels of Bcl-2 and BAX were examined by Western blot. Oridonin inhibited the growth of CEM cells in time- and dose dependent manner and the ICs0 of Oridonin was (7. 37± 1. 99) μmol/L after 72 h treatment. The cellular membrane of CEM cells treated with Oridonin became unsharp, some of them disintegrated. Oridonin induced apoptosis in CEM cells and the percent of apoptosis rate after 0, 5, 7.5, 10 μmol/L Oridonin treatment for 24 h were (4. 8±2. 11)%, (19.03±12.54)% ,(40.27± 3.31) / and (57. 23 ± 6. 69)% respectively. Oridonin inhibited activation of mTOR, P70S6, 4EBP1, RAF. ERK and STAT5 signaling protein, which were constitutively activated in CEM cells, however, Oridonin had no inhibitory effect on AKT kinase. Oridonin down-regulated the level of anti apoptotic protein Bcl-2 and up-regulated the expression of pro-apoptotic protein Bax.
CONCLUSIONS:
Oridonin exerted antileukemia effect in CEM cells by inhibiting the activation of mTOR/P70/4EBP1, RAF/ERK and STATS signaling pathways, down-regulating the expression of Bel-2 and up-regulating the expression of BAX.
Zhong Yao Cai. 2014 Jul;37(7):1230-3.
Experimental study on anti-pancreatic cancer effect of oridonin.
To investigate the apoptotic effect of Oridonin in human pancreatic cancer cells PANC-1, and to explore the underlying mechanism.
METHODS AND RESULTS:
MTT assay was used to measure the cell viability. Apoptosis was determined by confocal laser scanning microscope after Hoechst 33342 staining and flow cytometry analysis after PI staining. The regulation of JNK and p38 MAPK signaling pathway proteins was examined by Western blot analysis. Treatment with Oridonin for 24 h resulted in a marked decrease in cell viability in a dose-dependent manner. The IC50 value was determined as 49.80 μmol/L for 24 h. After treatment with 50 micromol/L and 80 μmol/L Oridonin for 24 h, typical apoptotic nucleus alterations were observed with confocal laser scanning microscope and apoptotic rates of PANC-1 cells increased by flow cytometry analysis. Treatment with 80 μmol/L Oridonin down-regulated protein expression of JNK, p38 and increased the expression of p-JNK, p-p38. Furthermore, 80 μmol/L Oridonin treatment decreased the expression of down-stream proteins Caspase-9, Caspase-3 and PARP in the apoptotic pathway as well as activated the cleavage of Caspase-9.
CONCLUSIONS:
Oridonin can induce apoptosis of PANC-1 cells through JNK and p38 MAPK pathway proteins.
HPLC of Forskolin
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
113.2900
1.4520
1.4520
.2675
1.3649
5.1468
High
42.0675
4.9011
No
No
No
No
No
No
0.0
Yes
No
Yes
Yes
Forskolin, also known as Coleonol, is a natural diterpenoid compound extracted from the roots of the Lamiaceae plant Coleus forskohlii. Since its first isolation and identification in the 1970s, Forscolin has attracted widespread attention due to its unique biological activity, especially as an effective activator of adenylate cyclase (AC). It can significantly promote the production of cyclic adenosine phosphate (cAMP) within cells, thereby regulating various cellular signaling pathways and affecting cell metabolism, differentiation, and functional status. In recent years, with in-depth research into the cAMP signaling pathway in various physiological and pathological processes, the potential application value of Forscolin in cardiovascular diseases, ophthalmic diseases, metabolic disorders, tumors, and neurodegenerative diseases has gradually emerged.
This paper aims to systematically review the chemical structure and physicochemical properties of Forscolin, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation and pharmacokinetic characteristics, as well as its clinical application prospects and future research directions, providing reference and reference for researchers in the field of natural product pharmacology.
The chemical name of Forscolin is 7-β-hydroxy-8,13-bicycloditerpene-1,6-dione, with the molecular formula C22H34O7 and a molecular weight of 410.5070. Its structural core is a diterpene framework containing multiple hydroxyl and ketone groups, characterized by high polarity and complex stereochemical characteristics. Forscolin has a LogP value of about 1.452, indicating moderate lipid solubility that facilitates penetration of cell membranes. The topological pole surface area (TPSA) is 113.29 Ų, indicating that it possesses certain polarity and hydrogen bond donor/acceptor capabilities, which is significant for binding to biological macromolecule targets.
Low water solubility (0.2675 mg/mL) limits its solubility in aqueous media and affects its bioavailability. Notably, Forscolin has good blood-brain barrier permeability, suggesting its potential application value in central nervous system diseases. In terms of safety, Forscolin did not show hERG channel inhibitory activity, and the Ames-induced mutagenic test was negative, indicating a solid safety foundation.
Forskohlii mainly comes from the Indian umbrella flower (Coleus forskohlii briq.), a perennial herbaceous plant widely distributed in India, Nepal, and Southeast Asia. The plant's roots are rich in forscolin, an important component of traditional herbal medicine. Traditionally, Indian umbrella root has been used to treat heart disease, hypertension, and digestive system disorders.
Forscolin is usually extracted using organic solvent extraction. Common solvents include methanol, ethanol, ethyl acetate, etc. Combining ultrasound-assisted extraction or reflux extraction techniques can improve extraction efficiency. The extract is concentrated, liquid-liquid dispensed, and purified by column chromatography to obtain high-purity Forscolin. In recent years, supercritical CO2 extraction and membrane separation technologies have also been introduced to achieve green and efficient extraction.
The optimization of extraction processes not only increases yield but also ensures the stability of the active ingredients in Forscolin, laying the foundation for large-scale production and pharmaceutical development.
As an adenylate cyclase activator, Forscolin can significantly increase intracellular cAMP levels, regulate various cAMP-dependent signaling pathways, and exhibit diverse pharmacological activities.
Cardiovascular system function
Forscolin activates AC, increases cAMP, promotes calcium influx in myocardial cells, produces positive inotropic effects, and enhances cardiac contractility. Additionally, its effects of dilating blood vessels and reducing peripheral resistance help lower blood pressure. Animal experiments have shown that Forscolin can effectively improve cardiac function in heart failure models and has potential cardiovascular protective effects.
Platelet antiaggregation effect
Forscolin inhibits platelet activation and aggregation through the cAMP pathway, reducing the risk of thrombosis. This characteristic gives it potential for application in preventing thrombotic diseases.
Lowers intraocular pressure
Forscolin can regulate the production and discharge of intraocular aqueous humor, lowering intraocular pressure. Related targets include carbonic anhydrases (CA2, CA4, CA12), adenylate cyclase (ADCY5), phosphodiesterase 4B (PDE4B), and cAMP-dependent protein kinase (PRKACA). Its ability to lower intraocular pressure offers new approaches for glaucoma treatment.
Cell differentiation and autophagy induction
Forskolin can induce differentiation of various cell types, promoting tissue repair and regeneration. At the same time, by activating the cAMP/PKA signaling pathway, it induces autophagy, participating in intracellular metabolic homeostasis regulation and cellular protection under pathological conditions.
Nuclear receptor activation
Forscolin activates pregnane X receptor (PXR) and farniestate X receptor (FXR), regulates drug metabolism enzymes and bile acid metabolism, and affects liver detoxification and lipid metabolism, suggesting its potential application in metabolic diseases.
The core mechanism of action of Forscolin is the activation of adenylate cyclase, especially type I AC, with an IC50 of about 41 nM and an EC50 of about 0.5 μM. Through this mechanism, Forscolin promotes the conversion of ATP to cAMP, activates cAMP-dependent protein kinase A (PKA), and thereby regulates the activity of downstream signaling molecules such as CREB (cAMP responsive factor binding protein) transcription factors, thereby modulating gene expression.
In addition, Forscolin affects several related targets:
Through the synergistic effects of these multiple targets, Forscolin exerts comprehensive regulatory effects across multiple physiological and pathological processes.
The physicochemical properties of Forscolin indicate that it has certain potential as a pharmaceutical product. With a molecular weight of 410.5, moderate lipid solubility (LogP 1.452), and high polarity (TPSA 113.29), it offers advantages in cell membrane penetration and targeted binding. Low water solubility limits its oral bioavailability and requires pharmaceutical improvement.
In terms of safety, Forscolin does not suppress hERG channels, and the Ames test is negative, indicating lower cardiotoxicity and mutagenic risk.
Pharmacokinetic studies show that forscolin is absorbed orally relatively quickly, but its bioavailability is limited by first-pass effects and solubility. It is widely distributed in the body, especially able to cross the blood-brain barrier, suggesting its potential applications for central nervous system diseases. The metabolic pathway mainly involves liver enzymes, and excretion is primarily through bile and urine.
To enhance its clinical value, current research focuses on formulation optimization, such as nanocarriers, liposome encapsulation, and eutectic technologies, to improve stability and bioavailability.
Due to its multi-target and multi-pathway pharmacological activity, Forscolin shows broad application prospects across multiple clinical fields:
Glaucoma and ophthalmic diseases
Forscolin lowers intraocular pressure by regulating the production and drainage of aqueous humor in the eye, making it a potential candidate for glaucoma treatment. Its mechanism of action is unique and is expected to be used in combination with existing drugs to improve efficacy.
Cardiovascular diseases
Its positive muscle strength and antihypertensive effects give Forscolin therapeutic potential in conditions such as heart failure and hypertension. In the future, combining modern drug delivery technologies is expected to develop novel cardiovascular drugs.
Metabolic diseases
By activating PXR and FXR, Forscolin regulates lipid metabolism and drug-metabolizing enzymes, and may be used for metabolic disorders such as nonalcoholic fatty liver disease (NAFLD) and hyperlipidemia.
Tumors and neurological diseases
The role of induced cell autophagy and differentiation offers new ideas for cancer treatment and neurodegenerative diseases. Its ability to cross the blood-brain barrier provides a foundation for drug development in the central nervous system.
Future research should focus on deeply elucidating the molecular mechanisms of forscolin, optimizing its pharmacokinetic characteristics, conducting more preclinical and clinical trials, and verifying its safety and efficacy.
As a classic natural product, Forscolin holds significant value in pharmacology due to its unique adenylate cyclase activation function and multi-target mechanism of action. Its potential applications in cardiovascular, ophthalmic, metabolic, and neurological diseases show broad prospects for clinical translation. In the future, combining modern medicinal chemistry and formulation technologies, Forscolin is expected to become a novel drug for treating various diseases. Systematic and in-depth mechanistic research and clinical validation will provide a solid foundation for drug development and promote the continued advancement of natural product pharmacology.
Shenshuai
Wenjing
Hedandan
