Common Name(s): N-(2-furanylmethyl)-1H-purin-6-amine, 6-furfurylaminopurine, Kinetin, Kinetin riboside, N6-furfuryladenine
Kinetin, initially thought to be a synthetic product, was isolated over 50 years ago as a plant hormone or cytokinin. Cytokinins function as essential growth hormones that can influence cell growth and differentiation in plant and nonplant tissues. Kinetin is found in plant cell extracts, including plant root nodules and the endosperm liquid of fresh, young coconut fruit. It has also been identified in freshly extracted DNA from human cells, human urine, and herring sperm.1
One of the first recognized cytokinins was a component of coconut milk, which was used as a standard additive to plant tissue cultures because of its ability to induce plant cell division (cytokinesis). Studies dating back to the mid-1950s describe the structure and synthesis of the cytokinin kinetin.1, 2
Cytokinins are N6-substituted adenine derivatives, categorized into 3 groups: the isoprenoid, the aromatic cytokinins, and the furfural group consisting of kinetin and kinetin riboside. Kinetin is thought to originate from furfural, a primary oxidation product of the deoxyribose in DNA. Kinetin exhibits electrochemical properties, which facilitate its measurement in biological material. A review of the chemical structure of kinetin and its associated moieties has been published.1, 2, 3
Uses and Pharmacology
Most studies utilize the kinetin riboside because free-base cytokinins are weaker cytotoxic agents, with the ribose at N9 of the purine ring essential for activity.2 Suppression of cellular signaling, cell-cycle arrest, and induction of apoptosis have been demonstrated in vitro.2, 3, 4, 5, 6, 7
Clinical studies are lacking. In vitro studies have shown efficacy of kinetin riboside against human cell cancer lines, including leukemia, melanoma and hepatoma, and breast and prostate cancers.2, 3, 5, 6
In vitro studies in plant and human cells, including keratinocytes, have shown that kinetin modulates cell growth. Varying concentrations of kinetin have inhibiting and modulating effects on different stages of cell development.7, 8, 9, 10, 11 Kinetin is reported to have delayed aging and prolonged the lifespan of the fruitfly.12
Topical application of kinetin to aged skin in hairless dogs for 100 days resulted in skin rejuvenation and depigmentation.1 No photoprotection was shown by either topical kinetin 0.1% or 0.5% on pig skin patches.13
Quality clinical trial data are lacking. Information on the purported antiaging effects of kinetin is largely limited to company-sponsored, open-label studies, which have not been published in peer-reviewed journals. One small, open-label, sponsored clinical study in mild to moderate rosacea showed improvement in facial erythema, skin roughness, and hyperpigmentation, but there was no effect on facial inflammatory pustules. In the absence of a control group, it is difficult to attribute the results to either the kinetin or the moisturizing vehicle itself.14 A double-blind, controlled study evaluating the effect of kinetin 0.03% with niacinamide over niacinamide alone found a trend toward improvement of facial aging for the kinetin study group.15
Familial dysautonomia is an autosomal recessive human genetic disorder caused by faulty RNA splicing that leads to impaired development of sensory and autonomic nerves. Disease severity depends on the extent of impaired coding, and small shifts in splicing can halt disease progression and neurodegeneration. The potential for kinetin in familial dysautonomia was discovered in a screening program for neurological disorders and stroke, and a proposed mechanism of action has been described.16, 17, 18
Clinical trials are limited and have been primarily conducted to elucidate the pharmacokinetics of orally administered kinetin and its tolerability. Researchers have demonstrated the effect of kinetin in improving splicing in the plasma of familial dysautonomia patients; further clinical trials are needed to determine if kinetin is able to assert this effect in the CNS.18, 19
Kinetin has been shown to inhibit platelet aggregation in vitro and in mice. Bleeding times increased with administration of a kinetin bolus, possibly via inhibition of thromboxane A2 or free radical scavenging on the surface of activated platelets.1, 20
Pregnancy / Lactation
Information regarding safety and efficacy in pregnancy and lactation is lacking. In vitro studies suggest nonmalignant cells may also be affected by the growth-suppressive effects of kinetin riboside.7
No clinical data are available. As bleeding times increased with administration of a kinetin bolus in mice, an interaction with antithrombotic agents might be anticipated with systemic use.20
Oral administration of kinetin has been studied in very limited trials. Patients reported nausea as kinetin dosages increased. Headache, rash, diarrhea, and tinnitus were uncommonly reported.18, 19 Information on adverse reactions due to topical application of kinetin is limited.1 Case reports of reactions to commercial topical preparations are lacking.
In rodents, only extremely high dosages were toxic.18 Information in humans is lacking; in limited clinical trials, modest reversible increases in liver enzymes were observed. A decreased platelet count was observed in 1 patient. No effect was observed on blood pressure, heart rate, weight, or neurological examination.18, 19
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