Product name: Teprenone
Synonym name: Geranylgeranylacetone [mixture of (5E,9E,13E)- and (5Z,9E,13E)- isomers]
Catalogue No.: BP2100
Cas No.: 6809-52-5
Formula: C23H38O
Mol Weight: 330.556
Botanical Source:
Type of Compound: Aliphatics
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.
For Reference Standard and R&D, Not for Human Use Directly.
HPLC of Teprenone
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
17.0700
7.6246
7.6263
.0007
7.7734
8.2821
High
92.1707
2.8364
Yes
Yes
No
No
No
No
0.0
No
Yes
Yes
Yes
Teprenone (CAS number: 6809-52-5), as a natural product derived compound with multiple pharmacological activities, has attracted widespread attention in recent years in the fields of ulcer prevention and multi-organ protection. Its main mechanism of action is to induce the expression of heat shock proteins (HSPs), especially Hsp70, thereby exerting cellular protective effects. Tepredone not only demonstrates remarkable efficacy in gastric mucosal protection and anti-ulcer treatment, but also demonstrates its potential to protect the liver, nervous system, kidneys, and heart, demonstrating its unique advantages as a multi-target drug. This paper will systematically review the chemical structure and physicochemical properties of tepredone, plant origin and extraction methods, pharmacological activity studies, mechanisms of action and molecular targets, druggability evaluation, and pharmacokinetic characteristics, and explore its clinical application prospects and future development directions.
Tepredone is a terpene ketone compound with a molecular formula of C_20H_34O and a molecular weight of 330.5560. Its structural feature is that the (9E,13E)-aninate group is bonded to one of the α-methyl groups of acetone, with two geometric isomers, 5E and 5Z, mixed in a 3:2 ratio. This compound belongs to the terpene and methyl ketone classes and contains typical geranile groups, giving it high hydrophobicity.
In terms of physicochemical properties, tepredone has a LogP value as high as 7.6246, indicating strong lipophilusibility and extremely low water solubility (0.0007), which significantly affects its in vivo distribution and pharmacokinetics. Its extremely low polar surface area (TPSA of 17.07) and high lipophilusibility make it easy to cross the blood-brain barrier (BBB), and experimental data confirm its high BBB penetration ability. Additionally, teprevone does not show hERG channel inhibitory activity, and its Ames mutagenic test was negative, indicating high safety and promising drug potential.
Teprevone was originally isolated from natural plant terpenoids, although its specific plant sources are relatively limited and it is usually prepared by semi-synthetic methods. Its parent structure mostly comes from natural products of geranifolyl terpenes, which are widely found in various aromatic plants, such as citronella oil and lemongrass oil.
The extraction method mainly relies on distillation of plant volatile oils, followed by separation and purification techniques such as column chromatography to obtain senillyl terpene precursors. The synthesis of tepredone mostly uses chemical synthesis routes, achieved through structural modification of geranial terpenes and the introduction of ketone groups. Modern manufacturing processes emphasize efficiency, green design, and controllability to meet the demands of industrial production.
Pharmacological activity studies of tepredone cover multiple aspects including anti-ulcer, liver protection, neuroprotection, renal protection, and cardiac protection.
As an anti-ulcer drug, tepredone mainly promotes the repair and protection of the gastric mucosa. Numerous in vivo and in vivo experiments have shown that tepredone can enhance the gastric mucosal barrier function, promote mucus secretion, inhibit excessive gastric acid secretion, and, by inducing Hsp70 expression, alleviates oxidative stress and inflammatory responses in gastric mucosal cells, thereby effectively preventing and treating gastritis and gastric ulcers.
Teprevone demonstrates significant protective effects in liver disease models, reducing liver cell damage and promoting liver cell regeneration. Its main mechanisms include antioxidant, anti-inflammatory, and regulation of apoptosis. By inducing Hsp70, tepredone enhances hepatocyte tolerance to various harmful stimuli, reducing the progression of liver fibrosis.
Neuroprotective effects are an emerging area in teprevone research. Research shows that tepredone can regulate heat shock protein expression within nerve cells, reduce neuroinflammation and oxidative stress, and protect neurons from damage, demonstrating potential therapeutic value in neurodegenerative diseases and cerebral ischemia-reperfusion injury models.
Tepredone also demonstrates protective effects for the kidneys and heart. In the kidney injury model, tepredone reduces tubular cell damage by inhibiting inflammatory factors and oxidative stress. In terms of heart protection, it can reduce myocardial ischemia-reperfusion injury, improve myocardial function, and prevent myocardial cell apoptosis.
The core mechanism of action of tepredone is to induce the expression of heat shock protein Hsp70, which acts as a molecular chaperone to stabilize protein structures, promote repair and degradation of damaged proteins, and enhance cellular tolerance to various stresses. Additionally, teprevone exerts its multi-target effect by modulating multiple signaling pathways.
Tepredone's therapeutic targets in gastritis and related diseases include:
Tepredone achieves its multi-protective effect by regulating these targets to inhibit inflammatory responses, reduce oxidative stress, and promote cell repair.
The action of tepredone involves multiple signaling pathways, especially the regulation of NF-κB and MAPK signaling pathways. By inhibiting NF-κB activation, teprevone reduces the expression of pro-inflammatory factors and alleviates inflammatory responses; By modulating the MAPK pathway, it promotes cell survival and repair. Additionally, teprevone activates the AKT signaling pathway, enhancing cell resistance to apoptosis.
Druggability evaluations of tepredone show that it has a solid foundation for safety and efficacy. Its high lipophilic solubility (LogP=7.62) may affect oral absorption, but it also facilitates penetration of biological membranes, especially the blood-brain barrier, supporting its neuroprotective effects. The low polarity surface area (TPSA=17.07) further enhances its membrane permeability.
Extremely low water solubility (0.0007) suggests that tepredone may be distributed in vivo toward a lipid environment, requiring appropriate formulation techniques to improve bioavailability. The high permeability of the blood-brain barrier gives it potential advantages in treating central nervous system diseases.
In terms of safety, teprevone did not show hERG channel inhibition, reducing the risk of cardiotoxicity; A negative Ames test indicates no significant mutagenicity and meets clinical drug safety requirements.
Pharmacokinetic studies show that tepredone is absorbed quickly after oral administration and is widely distributed, especially enriched in the liver and gastric mucosa. Its metabolism mainly occurs through hepatic enzyme systems, and the activity of these metabolites still requires further research. The excretion route is mainly bile and feces, with a moderate half-life, supporting routine dosing regimens.
As a multifunctional natural derivative drug, tepredone has been widely used in anti-ulcer clinical practice, especially showing good efficacy and safety in patients with gastritis and gastric ulcers. Its unique Hsp70 induction mechanism offers a new therapeutic strategy for traditional anti-ulcer drugs, especially suitable for gastric mucosal protection and repair.
In addition, teprexone is increasingly recognized for its potential in liver diseases, neurodegenerative disorders, kidney protection, and heart protection. In the future, with deeper analysis of its mechanism of action and optimization of pharmacokinetics, tepredone is expected to expand to more indications, especially in the comprehensive treatment of neurological diseases and multi-organ protection.
Improvements in formulation technologies, such as nanocarriers and liposome encapsulation, are expected to overcome their poor water solubility and enhance bioavailability and targeting. Combination therapy strategies are also a focus of future research, aiming to enhance treatment outcomes by combining them with anti-inflammatory and antioxidant drugs.
Clinical trial design needs further improvement, especially clinical validation targeting neuroprotection and hepatoprotection, to promote the expansion of Tepredone's indications and deepening clinical application.
Tepredone, as a unique terpene ketone natural derivative, demonstrates broad pharmacological activity and good safety due to its mechanism of inducing heat shock protein expression. Its successful application in ulcer treatment lays the foundation for future potential in liver, nerve, kidney, and heart protection. Through chemical modification, formulation optimization, and multi-target mechanism research, tepredone is expected to become an important drug in the field of multi-organ protection, providing new ideas and approaches for the treatment of related diseases. Ongoing basic and clinical research will further expand its clinical applications and benefit more patients.
