Activates and desensitizes transient receptor potential vanilloid subtype 1 (TRPV1) channel [1]

Inhibits transient receptor potential ankyrin 1 (TRPA1) channel [1]

Activates TRPM8 (cold receptor/minty-cool ion channel) [1]

Inhibits nicotinic acetylcholine receptors (nAChRs) (noncompetitive inhibition) [1]

Inhibits cytochrome P450 2B1 (CYP2B1) enzyme (IC50 = 7.89 μM using pentoxyresorufin-O-demethylase (PROD) as model substrate) [1]

Pure (1R)-(+)-camphor and (1S)-(-)-camphor tested individually exhibited negligible antifungal activity against Candida albicans [1]

(1R)-(+)-camphor and (1S)-(-)-camphor showed no antimicrobial activity against methicillin-resistant Staphylococcus aureus, Mycobacterium intracellulare, Cryptococcus neoformans, and Aspergillus fumigatus at a concentration of 200 μg/mL [1]

Camphor was found to have an inhibitory effect on pentoxyresorufin-O-demethylase (PROD), a model substrate for cytochrome P450 2B1 enzymes, with an IC50 value of 7.89 μM [1]

Camphor showed a positive result in the rec-assay using two strains of Bacillus subtilis, indicating possible DNA damage [1]

In a study using the repair-proficient strain of Escherichia coli, camphor reduced UV-induced mutagenesis and enhanced the formation of Lac+ recombinants, suggesting a protective effect through enhanced recombinational repair [1]

Camphor showed antimutagenic effects against UV-induced mutations in SY252 and D7 strains at very low concentrations (about 40% reduction of UV-induced revertant at 0.5 and 1 μg/plate), although higher concentrations failed to increase the effect [1]

Camphor reduced UV/4NQO mutagenesis in the NER+ strain of Escherichia coli, but not in the NER- strain [1]

Camphor increased spontaneous and UV-induced recombination in recA730 and recA+ cells [1]

Low doses of camphor were antigenotoxic against 4NQO in mammalian cells and stimulated DNA repair [1]

Camphor (1.2 μg/mL) did not show antiviral activity against herpes simplex virus-1 in Vero cells, but the essential oil rich in camphor showed virucidal activity with cytotoxicity [1]

Camphor, as a pure compound, showed contact and fumigant activity against Sitophilus oryzae and Rhizopertha dominica, but had no effect on Tribolium castaneum after 24 hours exposure at a dose of 0.1 μL/720 mL volume [1]

Camphor was found to markedly prevent the permeation of benzocaine across the skin while promoting skin accumulation after 12 hours in an in vitro permeation study using excised rat abdominal skin mounted in Franz diffusion cells [1]

Inhalation of camphor vapour at 500 mg/L significantly reduced cough frequency by 33% and increased cough latency in conscious guinea-pigs with citric-acid-induced cough [1]

Both camphor and camphor lactam were tested for antitussive activity in guinea-pigs with citric-acid-induced cough; prior exposure to camphor lactam at 125, 250, and 500 μg/L had a higher inhibitory cough response compared to camphor [1]

In a mouse bone marrow cell study, a single dose of camphor administered at 0.5 μM/g bodyweight significantly lowered the frequency of sister-chromatid exchanges (SCE) induced by gamma radiation [1]

Camphor (0.5 and 1 μg/plate) showed antimutagenic effects against UV-induced mutations in Saccharomyces cerevisiae (about 40% reduction) [1]

In insecticidal assays, camphor at 100 mg/filter paper and 100 μg/insect induced over 93% and 100% mortalities in Sitophilus granarius, S. zeamais and Prostephanus truncatus, but only 70% and 100% mortality in Tribolium castaneum after 24h exposure [1]

Development of eggs and immature stages within grain kernels, as well as progeny emergence, was completely inhibited in camphor-treated grain [1]

Camphor exhibited 78.5% mortality at the highest tested dose (10.0 μL/adult) for contact toxicity against Tribolium castaneum; for fumigant toxicity, camphor at its highest dose (120 μL/350 mL vol.) caused 93.5% mortality [1]

Camphor was the most effective of the tested monoterpenoids to prevent the multi-coloured Asian lady beetle, Harmonia axyridis, from overwintering in buildings as determined by olfactometer bioassay [1]

Camphor exhibited fumigation toxicity against Dinoderus bifloveatus after 48 hours exposure [1]

(1R)-(+)-camphor and (1S)-(-)-camphor were toxic against female Blattella germanica with LD50 values of 0.10 mg/cm² and 0.13 mg/cm², respectively, using the filter-paper contact toxicity bioassay; there was no significant difference in toxicity between the two enantiomers [1]

In a study on male rats, camphor administered at 50 mg/kg enhanced sexual desire and performance, as measured by mount latency and frequency and intromission latency and frequency [1]

Camphor fed at 119 ppm protected weight gains and protected against Eimeria tenella and Eimeria acervulina in chickens [1]

In a study on the cardiovascular effects of (+)-camphor in orthostatic hypotension using double-blind, randomised, placebo-controlled studies, (+)-camphor contributed to pressoric effects, inducing an initial rapid effect [1]

The inhibition of cytochrome P450 2B1 (CYP2B1) by camphor was evaluated using pentoxyresorufin-O-demethylase (PROD) as a model substrate. The reaction mixture contained rat liver microsomes as the enzyme source. The IC50 value for camphor was determined to be 7.89 μM [1]

The biosynthesis of camphor was investigated in Salvia officinalis. Geranyl diphosphate (GPP) is the preferred substrate. Cyclisation of GPP by (+)-bornyl diphosphate synthase yields (+)-bornyl diphosphate. (+)-Bornyl diphosphate is then hydrolysed to (+)-borneol through the action of bornyl-diphosphate diphosphatase. The final step is catalysed by (+)-borneol dehydrogenase, which oxidises (+)-borneol to (+)-camphor [1]

The antimicrobial activity of camphor was tested using the liquid diffusion method against Enterococcus hirae, Candida albicans, and Saccharomyces cerevisiae. The essential oil containing 44% camphor showed significant activity, but pure camphor was not separately tested [1]

The antibacterial and antifungal activities of camphor were determined against a variety of micro-organisms using disc diffusion and broth dilution methods. Camphor was found to be active, with notable activity against C. albicans and C. krusei in fractions [1]

The antiviral activity of camphor was assessed using plaque reduction assays. Camphor-rich essential oil from Santolina insularis deactivated HSV-1 and HSV-2 with IC50 values of 0.88 μg/mL for HSV-1 and 0.7 μg/mL for HSV-2. Reduction of plaque formation assays showed inhibition of cell-to-cell transmission of both HSV-1 and HSV-2 [1]

The cytotoxic activity of camphor was evaluated on African Green Monkey kidney (Vero) cells. Camphor, along with other components, exhibited cytotoxic activity [1]

The antimutagenic effect of camphor was tested using the repair-proficient strain of Escherichia coli and UV-induced mutagenesis. Camphor reduced UV-induced mutagenesis and enhanced the formation of Lac+ recombinants, but not as a consequence of SOS induction [1]

The inhibitory potential of camphor on UV-induced mutations was tested with SY252 and D7 strains of Saccharomyces cerevisiae. Camphor showed antimutagenic effects at very low concentrations (about 40% reduction of UV-induced revertant at 0.5 and 1 μg/plate) [1]

The genotoxicity modulation by camphor was studied in Escherichia coli NER+ and NER- strains and in mammalian cells. Camphor reduced UV/4NQO mutagenesis in the NER+ strain but not in the NER- strain, and increased spontaneous and UV-induced recombination in recA730 and recA+ cells [1]

The antigenotoxic effect of low doses of camphor against 4NQO was demonstrated in mammalian cells, where it stimulated DNA repair [1]

The antileishmanial activity of an essential oil containing 27.40% camphor was evaluated against promastigote (MIC 0.0097 μL/mL) and axenic amastigote forms (EC50 0.24 nL/mL) of Leishmania aethiopica and L. donovani. A weak haemolytic effect with a slightly decreased selectivity index (SI = 0.8) against the THP-1 cell line was also observed [1]

For the antitussive study, conscious guinea-pigs were exposed to camphor vapour at concentrations of 50, 133, and 500 mg/L. Cough was induced by citric acid. The 500 mg/L camphor significantly reduced cough frequency by 33% and increased cough latency [1]

For the antimutagenic study in vivo, camphor was administered as a single dose at 0.5 μM/g bodyweight to mice. Bone marrow cells were then examined for sister-chromatid exchanges (SCE) after exposure to gamma radiation [1]

For insecticidal contact toxicity assays, camphor was applied at doses of 100 mg/filter paper and 100 μg/insect against Sitophilus granarius, S. zeamais, Prostephanus truncatus, and Tribolium castaneum. Mortality was recorded after 24h exposure [1]

For insecticidal fumigant toxicity, camphor was tested at a dose of 120 μL/350 mL volume against Tribolium castaneum, resulting in 93.5% mortality [1]

For cockroach toxicity, female Blattella germanica were exposed to (1R)-(+)-camphor and (1S)-(-)-camphor using the filter-paper contact toxicity bioassay. LD50 values were calculated as 0.10 mg/cm² for (1R)-(+)-camphor and 0.13 mg/cm² for (1S)-(-)-camphor [1]

For the study on sexual activity, male rats were administered camphor at 50 mg/kg. Parameters measured included mount latency and frequency as well as intromission latency and frequency [1]

For the coccidia infection study, camphor was fed to chickens at 119 ppm as a supplement to protect weight gains and against Eimeria tenella and Eimeria acervulina [1]

For reproductive toxicity studies, pregnant rats were orally administered (+)-camphor at doses up to 1,000 mg/kg bodyweight/day, and pregnant rabbits at doses up to 681 mg/kg bodyweight/day during the period of organogenesis [1]

Metabolism / Metabolites
Known metabolites of (+)-camphor include 5-exo-hydroxycamphor and 8-hydroxycamphor.

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In the human body, camphor is oxygenated to alcohol camphorol and then conjugated with glucuronic acid in the liver to become water-soluble before being excreted in the urine [1]

Following oral ingestion, high concentrations of camphor have been detected in the foetal brain, liver, kidney, blood, as well as in amniotic fluid [1]

Camphor crosses the placenta; fetuses lack the enzymes to hydroxylate and conjugate camphor with glucuronic acid [1]

The lethal dose of camphor in humans is reported to be 50-500 mg per kg bodyweight. Ingestion of 3.5 g can cause death, whilst 2.0 g causes toxic effects in adults leading to congestion of the gastrointestinal tract, kidney, and brain [1]

Characteristic symptoms of camphor poisoning after ingestion include nausea, vomiting, headache, dizziness, muscular excitability causing tremor and twitching, convulsions, and delirium depending on dosage. In severe overdose, status epilepticus persisting for several hours occurs, ultimately causing coma and death by asphyxia or exhaustion [1]

Camphor inhalation may cause irritation of mucous membranes above 2 ppm, and respiratory depression and apnoea may occur. Camphor can also cause skin and eye irritation on contact [1]

The United States Food and Drug Administration set a limit of 11% camphor in consumer products in 1983 and banned products labeled as camphorated oil, camphor oil, camphor liniment, and camphorated liniment completely [1]

In a study on rabbits, oral administration of different concentrations of camphor solution for ten days resulted in mild oedema, glomerulonephritis, glomerular lobulations, tubular necrosis, and congestion of blood cells. Histologically, camphor administration distorted and disrupted the cytoarchitecture of the kidney [1]

In pregnant rats, oral administration of (+)-camphor at a high dose of 1,000 mg/kg bodyweight/day caused toxic symptoms including clonic convulsions, pilo-erection, and reduced motility, but no retardations or malformations were observed. In pregnant rabbits, a high dose of 681 mg/kg bodyweight/day resulted in reduced body weight gain and food consumption, but no retardations or malformations were observed [1]

Central serous chorioretinopathy (CSCR) of the right eye was reported in a 50-year-old female who had used Chinese herbal medicinal patches containing camphor as the main ingredient for more than 20 years [1]

For sage (Salvia officinalis) oil containing camphor, 3.2 g/kg caused tonic-clonic convulsions in unanaesthetised rats resulting in death [1]

Camphor ingestion may lead to abortion as it crosses the placenta and foetuses lack the enzymes to hydroxylate and conjugate with glucuronic acid [1]

[1]. Camphor--a fumigant during the Black Death and a coveted fragrant wood in ancient Egypt and Babylon--a review. Molecules. 2013 May 10;18(5):5434-54.

Camphor oil is a colorless liquid with a characteristic odor. Flash point 125°F (52°C). Insoluble in water, its density is usually less than that of water. Its vapor is heavier than air. D-camphor is a colorless or white crystal. It can sublimate. Flash point 149°F (65°C). Flammable, with a bright and smoky flame. It has a strong aromatic odor. The taste is spicy and aromatic, followed by a cooling sensation. (NTP, 1992) (R)-camphor is the (R)-enantiomer of camphor. It is the enantiomer of (S)-camphor. D-camphor has been reported in Magnolia officinalis, Artemisia xerophytica, and other organisms with relevant data. See also: Coriander oil (partial); Camphor (note moved here).

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Camphor has been used as a fumigant during the Black Death (plague that spread through Europe in the 14th century), as well as during outbreaks of smallpox and cholera. Rosewater together with camphor as a perfume ingredient was sprinkled over corpses before shrouding [1]

In India, camphor is commonly burnt in temples during religious rituals because camphoric fumes are non-irritant to eyes [1]

Camphor has been widely used as a fragrance in cosmetics, as a flavouring food additive, as a preservative in confectionary goods, as an insect repellent, a plasticiser, and as an intermediate in the synthesis of aroma chemicals [1]

Camphor has an annual market value of 80-100 million US$ [1]

Camphor is used as a chiral starting material and auxiliary in asymmetric synthesis. It is used in the synthesis of α-amino acids, α-aminophosphonic acids, α-substituted benzylamines, α-amino alcohols, and aromatic steroids. Camphenesulfonic acid (camphor-derived) is useful for chiral reductions [1]

Camphor has been used as a skin penetration enhancer. In a study on the skin permeation of tea catechins, camphor showed the least enhancement among oxygen-containing monoterpenes, which may be related to its bicyclic structure. The rank order of enhancement was α-terpineol ≥ menthone > linalool > 1,8-cineole > farnesol ≥ fenchone > cymene ≥ nerolidol > (+)-limonene > camphor [1]

C10H16O

152.23

152.12

464-49-3

159055

White to off-white solid powder

1.0±0.1 g/cm3

207.4±0.0 °C at 760 mmHg

176-180ºC

64 ºC

0.2±0.4 mmHg at 25°C

1.485

2.13

0

1

0

11

217

2

C[C@@]12CC[C@@H](C1(C)C)CC2=O

DSSYKIVIOFKYAU-XCBNKYQSSA-N

InChI=1S/C10H16O/c1-9(2)7-4-5-10(9,3)8(11)6-7/h7H,4-6H2,1-3H3/t7-,10+/m1/s1

(1R,4R)-1,7,7-trimethylbicyclo[2.2.1]heptan-2-one

(R)-(+)-Camphor Japanese camphor Laurel camphorAI3-01698 AI3 01698AI301698 Formosa camphord-2-Bornanone

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 50 mg/mL (~328.45 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (16.42 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (16.42 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (16.42 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)