Common Name(s): N-(2-furanylmethyl)-1H-purin-6-amine, 6-furfurylaminopurine, Kinetin, Kinetin riboside, N6-furfuryladenine
Medically reviewed by Drugs.com. Last updated on May 2, 2022.
Kinetin has primarily been used topically as an antiaging preparation, although there is limited clinical information to support this use. Potential uses for oral kinetin include the treatment of genetic disorders such as familial dysautonomia and certain cancers.
Oral kinetin has only been studied in a few clinical trials of questionable quality. Topical applications are available at 0.03% to 0.1% strengths.
Contraindications have not yet been identified.
Information regarding safety and efficacy in pregnancy and lactation is lacking.
None well documented.
Information on adverse reactions due to topical application is limited. Case reports of reactions to commercial topical preparations are lacking.
Information is limited.
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.Barciszewski 2007
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.Barciszewski 2007, Voller 2010
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.Barciszewski 2007, Choi 2008, Voller 2010
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.(Voller 2010) Suppression of cellular signaling, cell-cycle arrest, and induction of apoptosis have been demonstrated in vitro.(Cabello 2009, Cheong 2009, Choi 2008, Dudzik 2011, Tiedemann 2008, Voller 2010)
Studies have been conducted in mice with induced melanoma and myeloma. Inhibition of the tumor growth has been demonstrated.(Choi 2008, Tiedemann 2008, Voller 2010)
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.(Cabello 2009, Cheong 2009, Choi 2008, Voller 2010)
Results on the neuroprotective effects of kinetin have been equivocal.(Orr 2017, Wei 2017) In Parkinson’s rat disease models, long-term oral administration of kinetin for 60 days did not affect the density of striatal dopamine neurons or protect against alpha-synuclein-induced dopaminergic neurodegeneration, pathological, or behavioral deficits. However, a reduction in weight was observed with prolonged administration of high levels of kinetin.(Orr 2017) In contrast, in an Alzheimer’s disease mouse model, kinetin significantly improved memory and spatial learning abilities in a dose-dependent manner (P<0.05 each), reduced aluminum levels in the cortex and hippocampus, and restored acetylcholine via inhibition of acetylcholinesterase.(Wei 2017)
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.(Berge 2006, Dudzik 2010, Karagiannis 1994, Kowalska 1992, Rattan 1994) Kinetin is reported to have delayed aging and prolonged the lifespan of the fruitfly.(Sharma 1995)
Topical application of kinetin to aged skin in hairless dogs for 100 days resulted in skin rejuvenation and depigmentation.(Barciszewski 2007) No photoprotection was shown by either topical kinetin 0.1% or 0.5% on pig skin patches.(Tournas 2006)
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.(Wu 2007) 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.(Chiu 2007)
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.(Axelrod 2011, Hims 2007, Lee 2011)
Studies in rodents have been undertaken to evaluate the distribution of orally administered kinetin.(Axelrod 2011, Gold-von Simson 2009)
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.(Axelrod 2011, Gold-von Simson 2009)
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.(Barciszewski 2007, Hsiao 2003)
Information is limited. Oral kinetin has been trialed in patients with familial dysautonomia at maximum dosages of 23.5 mg/kg/day for up to 28 days.Axelrod 2011, Gold-von Simson 2009
Topical applications are available at 0.03% to 0.1% strengths.Chiu 2007, Wu 2007
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.Dudzik 2011
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.Hsiao 2003
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.Axelrod 2011, Gold-von Simson 2009 Information on adverse reactions due to topical application of kinetin is limited.Barciszewski 2007 Case reports of reactions to commercial topical preparations are lacking.
In rodents, only extremely high dosages were toxic.Axelrod 2011 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.Axelrod 2011, Gold-von Simson 2009
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