Undecanoic acid (UDA) is a fatty acid with significant antimycotic activity. Undecanoic acid is a straight-chain, eleven-carbon saturated medium-chain fatty acid found in body fluids; the most fungitoxic of the C7:0 - C18:0 fatty acid series. It has a role as a human metabolite and an antifungal agent. It is a straight-chain saturated fatty acid and a medium-chain fatty acid. It is a conjugate acid of an undecanoate. It derives from a hydride of an undecane. Undecanoic acid inhibited the production of exocellular lipase and keratinase but stimulated the production of exocellular phospholipase A in T. rubrum undecanoic acid-resistant mutant (udar). At its minimum inhibitory concentration, undecanoic acid inhibits biosynthesis of phosphatidyl serine, phosphatidyl ethanolamine and polyphosphoinositol but does not inhibit the synthesis of phosphatidyl glycerol, phosphatidyl choline, phosphatidyl inositol and phosphatidic acid in Trichophyton rubrum. At higher concentration, however UDA inhibits biosynthesis of all phosphatides present in this dermatophyte. UDA also affects catabolism of these phosphatides. This inhibitory effect of UDA may be partially responsible for its toxic action on T. rubrum.

Vanillyl alcohol is a monomethoxybenzene that is 2-methoxyphenol substituted by a hydroxymethyl group at position 4. It has a role as a plant metabolite. It is a member of guaiacols and a member of benzyl alcohols. Vanillyl alcohol is a phenolic alcohol and is used as a flavoring agent in foods and beverages. Vanillyl alcohol effectively inhibited the cytotoxicity and improved cell viability in MPP+-induced MN9D dopaminergic cells. Vanillyl alcohol attenuated the elevation of reactive oxygen species (ROS) levels, decreased in the Bax/Bcl-2 ratio and poly (ADP-ribose) polymerase proteolysis. These results indicate that vanillyl alcohol protected dopaminergic MN9D cells against MPP+-induced apoptosis by relieving oxidative stress and modulating the apoptotic process and is therefore a potential candidate for treatment of neurodegenerative diseases such as Parkinson's disease.

https://translate.google.ru/#view=home&op=translate&sl=en&tl=ru&text=Pyrrole%20is%20a%20five-membered%20aromatic%20heterocyclic%20compound%2C%20which%20contains%20one%20nitrogen%20atom.%20Pyrrole%20is%20a%20colorless%20volatile%20liquid%20that%20darkens%20readily%20upon%20exposure%20to%20air%20and%20is%20usually%20purified%20by%20distillation%20immediately%20before%20use.%20Due%20to%20its%20aromatic%20character%2C%20pyrrole%20is%20difficult%20to%20hydrogenate%2C%20does%20not%20easily%20react%20as%20a%20diene%20in%20Diels%E2%80%93Alder%20reactions%2C%20and%20does%20not%20undergo%20usual%20olefin%20reactions.%20Its%20reactivity%20is%20similar%20to%20that%20of%20benzene%20and%20aniline%2C%20in%20that%20it%20is%20easy%20to%20alkylate%20and%20acylate.%20Under%20acidic%20conditions%2C%20pyrroles%20polymerize%20easily%2C%20and%20thus%20many%20electrophilic%20reagents%20that%20are%20used%20in%20benzene%20chemistry%20are%20not%20applicable%20to%20pyrroles.%20Pyrrole%20and%20its%20derivatives%20(pyrroles)%20are%20widely%20used%20as%20an%20intermediate%20in%20the%20synthesis%20of%20pharmaceuticals%2C%20medicines%2C%20agrochemicals%2C%20dyes%2C%20photographic%20chemicals%2C%20perfumes%2C%20and%20other%20organic%20compounds.%20For%20example%2C%20chlorophyll%20and%20heme%20are%20the%20derivatives%20which%20are%20made%20by%20four%20pyrrole%20ring%20formation%20of%20the%20porphyrin%20ring%20system.%20Pyrrole%20is%20a%20precursor%20to%20the%20nonsteroidal%20anti-inflammatory%20drug%20tolmetin.

Tributyrin is a prodrug of natural butyrate. It is a neutral short-chain fatty acid triglyceride that is likely to overcome the pharmacokinetic drawbacks of natural butyrate as a drug. Tributyrin has potent antiproliferative, proapoptotic and differentiation-inducing effects in neoplastic cells. Compared with butyrate, tributyrin has more favorable pharmacokinetics and is well tolerated. Because it is rapidly absorbed and chemically stable in plasma, tributyrin diffuses through biological membranes and is metabolized by intracellular lipases, releasing therapeutically effective butyrate over time directly into the cell. Tributyrin may, at least in part, exert its growth-reducing and differentiation-inducing effect in Caco-2 cells by an upregulation of the vitamin D receptor; this may provide a useful therapeutic approach in chemoprevention and treatment of colorectal cancer. In phase I study of the orally administered tributyrin there was no consistent increase in hemoglobin F. Peak plasma butyrate concentrations occurred between 0.25 and 3 h after dose. Development of tributyrin as an anticancer agent was discontinued.

The monoterpene perillyl alcohol (POH) is a naturally occurring compound derived from citrus fruits, mint, and herbs. It exhibited chemotherapeutic potential against various malignant tumors in preclinical models and was being tested in clinical trials in patients with refractory advanced cancers. POH was formulated in soft gelatine capsules and orally administered to cancer patients several times a day on a continuous basis. However, such clinical trials in humans yielded disappointing results, also because of the large number of capsules that had to be swallowed caused hard-to-tolerate intestinal side effects, causing many patients to withdraw from treatment due to unrelenting nausea, fatigue, and vomiting. The clinical trials in Brazil have explored intranasal POH delivery as an alternative to circumvent the toxic limitations of oral administration. In these trials, patients with recurrent malignant gliomas were given comparatively small doses of POH via simple inhalation through the nose. Results from these studies showed, that this type of long-term, daily chemotherapy was well tolerated and effective. The precise mechanism of action is still undetermined, but it is known, that perillyl alcohol plays an important role in the process of hepatoma cell invasion and migration via decreasing the activity of Notch signaling pathway and increasing E-cadherin expression regulated by Snail. Another possible mechanism is included inhibition of Na/K-ATPase (NKA). The NKA α1 subunit is known to be superexpresses in glioblastoma cells (GBM) and POH acts in signaling cascades associated with NKA can control cell proliferation and/or cellular death.