Fibroblast proliferation is induced by camphor brain via PI3K/AKT and ERK signaling [3]. According to MTT assay results, brain fibroblast viability was increased to 108.9± at 32.5, 65, 130, and 260 μM Camphor as opposed to 6.6%, 118.6±2.8%, 127.7±4.2%, and 131.6±7.2% at 0 μM Camphor brain treatment[3]. The application of camphor (0-260 μM) therapy resulted in a 24-hour rise in ROS production of up to 17.97%, as opposed to 5.04% in the untreated laboratory [3]. The phosphorylation of PI3K, AKT, ERK, and 4EBP1 is activated by camphor (0-260 μM) in a time- and dose-dependent manner [3].

Cell Viability Assay[3]
Cell Types: primary dermal fibroblasts
Tested Concentrations: 0-260 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: 32.5, 65, 130 and 260 μM increased fibroblast viability to 108.9±6.6%, 118.6± 2.8%, 127.7±4.2% and 131.6 compared to 0 μM treatment, respectively ±7.2%.

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Western Blot Analysis[3]
Cell Types: Primary Dermal Fibroblasts
Tested Concentrations: 0-260 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: Induction of PI3K, AKT, ERK and 4EBP1 (mRNA translation repressor and mTOR substrate) in a Phosphorylation in a dose- and time-dependent manner.

Absorption, Distribution and Excretion
Camphor is rapidly absorbed by mucous membranes and the gastrointestinal tract. It can also be absorbed through inhalation, skin application, and nasal instillation. Following maternal ingestion of camphor, it is detectable in maternal blood within 15 minutes but becomes undetectable after 8 hours. At delivery 36 hours later, camphor is detected in amniotic fluid, umbilical cord blood, fetal blood, and in the fetal brain, liver, and kidneys. The digestion and absorption of pure camphor or camphor alcohol solutions is quite rapid, but absorption of camphor oil preparations is slower. Camphor is slowly absorbed subcutaneously or intramuscularly. Absorbed camphor is primarily excreted in urine as oxidized camphor alcohol, but small amounts are also found in respiration, sweat, and feces. For more complete data on the absorption, distribution, and excretion of camphor (7 species), please visit the HSDB records page. Metabolism/Metabolites Two induction phases were observed in the liver microsomes of female mice after inhalation of DL-camphor. The apparent molar activity of ethyl umbelliferone dealkylase decreased within the first 24 hours. In the second phase, the molar activity of ethyl umbelliferone dealkylase remained unchanged. The metabolism of (+)-camphor and (-)-camphor was investigated in rabbits after administration via gastric tube; metabolites of (+)-camphor included (+)-borneol, (+)-5-hydroxycamphor, and (+)-3-hydroxycamphor. Camphor was rapidly oxidized to camphor alcohol (2-hydroxycamphor and 3-hydroxycamphor), which then conjugated with glucuronic acid in the liver to form glucuronide. Camphor-related metabolites are relatively lipid-soluble and may accumulate in adipose tissue. Biological half-life: 167 minutes (200 mg camphor alone); 93 minutes (200 mg camphor with solvent Tween 80).

Toxicity Summary
Identification and Uses: Camphor is a solid, translucent white crystalline powder with a pungent aromatic odor, used as an erythematous/irritant. It is also used in liniments for fibromyalgia, neuralgia, and similar conditions as an irritant. In dermatology, when camphor is used in emulsion form (0.1% to 3%), it has antipruritic and topical anesthetic effects (producing a cooling sensation upon gentle application). Camphor is no longer used as an insecticide in the United States. Other uses of camphor include its use as an insect repellent (especially for controlling clothes moths) and as a cosmetic ingredient. Human Exposure and Toxicity: The primary target organs for camphor exposure are the central nervous system and the kidneys. Ingestion of camphor may result in seizures, depression, respiratory arrest, cardiac arrest, gastric irritation, colic, nausea, vomiting, diarrhea, anxiety, excitement, delirium, and severe post-convulsive coma. Symptoms may appear within 5 to 90 minutes after ingestion, depending on the camphor product ingested (solid or liquid). The initial stage of camphor poisoning presents as excitement, accompanied by vomiting, diarrhea, and excitation, followed by central nervous system depression and death. Symptoms typically appear after ingestion of approximately 2 grams of camphor (lethal dose for adults: 4 grams, children: 0.5-1 gram, infants: 70 mg/kg pure camphor). There have been reports of infants fainting immediately after camphor is applied to their nostrils. Camphor is irritating to the eyes, skin, and mucous membranes. Topical application of camphor to the skin has an analgesic effect. Ingestion of camphor has irritant and carminative properties (SRP: a drug used to reduce flatulence). It has also been used as a mild expectorant. Camphor is a central nervous system stimulant, with effects ranging from mild excitation to grand mal seizures or status epilepticus. These effects stem from excitation of the brain and lower central nervous system structures. Gastric irritation, as well as excitation of the cortex and medulla oblongata, often lead to vomiting and diarrhea. It is currently unclear whether the toxicity of camphor is due to its parent compound, metabolites (secondary alcohols, including isomers of borneol and hydroxycamphor), or a combination of both. Camphor's use relies entirely on its local effects. When applied to the skin, it acts as an erythematous agent, causing local vasodilation (mediated by axonal reflex), resulting in a comfortable and warm sensation. As an antipruritic, gentle application to the skin produces a cooling sensation and mild local anesthetic effect, which may be followed by numbness. Small amounts can produce a warm and comfortable feeling in the stomach, but large doses are irritating. Camphor is not a human carcinogen, and topical use of camphor oil during pregnancy has not been found to have teratogenic effects. However, camphor ingestion may lead to miscarriage and/or fetal death because camphor can cross the placenta, and the fetus lacks the enzymes required for hydroxylation and glucuronic acid binding. Animal studies: Carcinogenicity tests in animals were negative. Repeated administration induced neuronal necrosis in mice. In developmental studies, oral administration of D-camphor at doses up to 1000 mg/kg body weight/day to pregnant rats during organogenesis and at doses up to 681 mg/kg body weight/day to pregnant rabbits did not show teratogenicity. Camphor did not show mutagenicity in the Ames test, but there are reports of sister chromatid exchange in mice injected intraperitoneally with 80 mg/kg camphor, suggesting that it may have genotoxicity.

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Interactions
This study evaluated the control efficacy of five plant volatile oils and their mixtures against the magrodidier wasp (Icerya seychellarum seychellarum (Westw.)) parasitizing sago palms in the Antoniades Public Garden in Alexandria, Egypt. The tested volatile oil concentrations were 0.5%, 1%, and 1.5% (v/v), with the following compositions: camphor 20%, dill 20%, rose 30%, peppermint 20%, and clove 30% (v/v). Their mixtures were: camphor/peppermint, camphor/rose (1:1), camphor/rose/peppermint (1:1:2), and camphor/rose/dill (2:1:1). The overall average percentage reduction in residues over the entire test period indicated that camphor and rose volatile oils were most effective in reducing mealybugs, followed by dill and peppermint, while clove volatile oil was the least effective. Evaluation of volatile oil mixtures showed that camphor/rose/mint, camphor/rose, and camphor/mint mixtures ranked highly effective against mealybugs. /Mixtures/
This study aimed to examine the anti-genotoxicity of plant monoterpenes—camphor, eucalyptol, and thujone—in prokaryotic and eukaryotic cells and to elucidate their effects on DNA repair. /Study/ The effects of monoterpenes on spontaneous mutations, UV radiation, and 4-nitroquinoline oxide (4NQO)-induced mutations were compared in *Escherichia coli* strains with normal K12 repair function and strains deficient in mismatch repair (MMR) and nucleotide excision repair (NER). Tannins and vanillin were included as positive controls in the bacterial assay. The study also examined the protective effect of monoterpenes against 4NQO-induced genotoxicity in Vero cell lines using an alkaline comet assay. Results obtained in strains with normal repair function indicated that monoterpenes have anti-mutagenic potential against UV radiation and 4NQO-induced mutations, but NER deficiency reduced this potential. Camphor and eucalyptol prolonged the UV-induced SOS response time, while thujone decreased the SOS response and reduced protein synthesis and cell growth rate. All three monoterpenoids increased spontaneous and UV-induced recombination in recA730 cells, with camphor also additionally increasing recA(+) cell recombination. Incubation of Vero cells pretreated with 4NQO with monoterpenoids significantly reduced comet tail moments. However, higher concentrations of monoterpenoids induced DNA strand breaks. These results indicate that camphor, eucalyptol, and thujone can stimulate error-free DNA repair processes by causing minimal DNA damage and act as biological antimutagenic agents. …Administering a single dose of camphor (0.5 μM/g body weight) 30, 45, or 60 minutes before irradiation significantly reduced the frequency of radiation-induced sister chromatid exchange (SCE); this effect was enhanced with increasing time intervals.

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Non-Human Toxicity Values
Oral LD50 in mice: 1310 mg/kg; Subcutaneous LD50 in rats: 70 mg/kg; Intraperitoneal LD50 in mice: 3000 mg/kg

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Toxicity Data
LCLo (mice) = 400 mg/m3/3H

[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.

[2]. Different ligands of the TRPV3 cation channel cause distinct conformational changes as revealedby intrinsic tryptophan fluorescence quenching. J Biol Chem. 2015 May 15;290(20):12964-74.

[3]. Camphor Induces Proliferative and Anti-senescence Activities in Human Primary Dermal Fibroblasts and Inhibits UV-Induced Wrinkle Formation in Mouse Skin. Phytother Res. 2015 Dec;29(12):1917-25.

Camphor is a colorless or white crystalline powder with a strong mothball odor. Its density is similar to water. It releases flammable gas at temperatures above 150°F (66°C). It is used in the manufacture of moth repellents, pharmaceuticals, and flavorings. Camphor is a cyclic monoterpene ketone, a compound of borneol with an oxygen substituent at the 2-position. It is a naturally occurring monoterpene compound that functions as a metabolite in plants. It is a borneol monoterpene compound and also a cyclic monoterpene ketone. Camphor is a bicyclic monoterpene ketone, widely found in plants, especially in the camphor tree (Cinnamomum camphora). It can be used externally for skin itch relief and anti-infection. The toxic effects of camphor appear rapidly after ingestion, and camphor oil is the most common cause of its toxicity. The U.S. Food and Drug Administration (FDA) has ruled that camphor oil cannot be sold in the United States, and that the concentration of camphor in any product must not exceed 11%. Camphor oil has been included in the list of drugs withdrawn or removed from the market due to safety and efficacy issues. However, camphor is present in low concentrations in many over-the-counter medications. Camphor has been reported in seaside calendula (Otanthus maritimus), riverbank winged bean (Tetradenia riparia), and several other organisms with relevant data. Camphor is a bicyclic monoterpene ketone widely found in plants, especially in the camphor tree (Cinnamomum camphora). It can be used topically for skin itch relief and anti-infection. See also: Camphor (synthetic) (note moved to); Camphor oil (note moved to). Camphor oil, white (note moved to)...see more...

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Mechanism of Action
Camphor is a natural compound and the main active ingredient in topical analgesic ointments and liniments. …Capsaicin and menthol are two other widely used topical medications for similar purposes, stimulating and desensitizing sensory nerves by acting on two members of the transient receptor potential (TRP) channel superfamily—the thermosensitive TRP vanillin subtype 1 (TRPV1) and the cold-sensitive TRP channel M8. Recent studies have shown that camphor can activate TRPV3, and the researchers in this paper found that camphor can also activate heterologously expressed TRPV1, but at a higher concentration than capsaicin. Phospholipase C-coupled receptor stimulation (mimicking an inflammatory state) enhances this activation. Similar camphor-activated TRPV1-like currents were observed in isolated rat dorsal root ganglion (DRG) neurons, and this current was significantly enhanced after activation of protein kinase C with phorbol-12-myristate-13-acetate (PMA). The channel region of rat TRPV1 activated by camphor differs from that of capsaicin, as evidenced by the fact that camphor can still activate TRPV1 in the presence of the competitive inhibitor capsaicin receptor antagonist (capsazepine) and in capsaicin-insensitive point mutants. Camphor failed to activate capsaicin-insensitive TRPV1 in chickens. TRPV1 desensitization is thought to contribute to the analgesic effect of capsaicin. The authors found that while camphor activated TRPV1 less efficiently, camphor application desensitized TRPV1 more quickly and thoroughly than capsaicin. Conversely, repeated camphor application sensitized TRPV3 currents, which is inconsistent with camphor's analgesic effect. The researchers also found that camphor inhibited several other related TRP channels, including ankyrin repeat TRP1 (TRPA1). Camphor-induced TRPV1 desensitization and TRPA1 blockade may be the mechanisms underlying camphor's analgesic effect.

C10H16O

152.2334

152.12

76-22-2

2537

White to off-white solid powder

1.0±0.1 g/cm3

207.4±0.0 °C at 760 mmHg

345 °F (NIOSH, 2024) ; 174-179 °C ; 180 °C ; 345 °F ; 345 °F

64.4±0.0 °C

0.2±0.4 mmHg at 25°C

1.485

2.13

0

1

0

11

217

0

CC1(C2CCC1(C(=O)C2)C)C

DSSYKIVIOFKYAU-UHFFFAOYSA-N

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

1,7,7-trimethylbicyclo[2.2.1]heptan-2-one

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 : ~100 mg/mL (~656.90 mM)
H2O : ~3.33 mg/mL (~21.87 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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Solubility in Formulation 4: 3.33 mg/mL (21.87 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication (<60°C).

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