According to reports, 6-methylcoumarin exhibits nearly negligible phototoxicity in test models for phototoxicity using epidermal tissue and cell culture. Four hours after treating HaCaT cells with 6-methylcoumarin (1-105 nM) and/or UVA (5 J cm-2), γ-H2AX was found using immunofluorescence labeling and Western blotting. Under UVA irradiation, 6-Methylcoumarin at a dose of 100 nM significantly generated γ-H2AX-positive cells [1].

Interactions
The following drugs may enhance the response to coumarin or indanedione derivatives: alcohol (acute poisoning), allopurinol, aminosalicylic acid, amiodarone, anabolic steroids, chloral hydrate, chloramphenicol, cimetidine, clofibrate, trimethoprim-sulfamethoxazole, danazol, dexthylexin sodium, diazoxide, diflunisal, disulfiram, erythromycin, ethacrynic acid, fenoprofen calcium, glucagon, ibuprofen, indomethacin, influenza vaccine, isoniazid, meclofenamic acid, mefenamic acid, methylthiouracil, metronidazole, miconazole, nalidixic acid, neomycin (oral), pentoxifylline, phenylbutazone, propoxyphene, propylthiouracil, quinidine, quinine. Salicylates, streptokinase, sulfinpyrazone, sulfonamides, sulindac, tetracyclines, thiazide diuretics, thyroid medications, tricyclic antidepressants, urokinase, vitamin E. /Coumarins and Indanedione Derivatives/
The following drugs...may...reduce...the response to coumarin or indanedione derivatives: alcohol (chronic alcoholism), barbiturates, carbamazepine, corticosteroids, adrenocorticotropic hormone, ethylclofenac, glutamine, griseofulvin, mercaptopurine, methylquinone, estrogen-containing oral contraceptives, rifampin, spironolactone, vitamin K. /Coumarins and Indanedione Derivatives/

---

Non-human toxicity values
Oral LD50 in rats: 1,680 mg/kg
Subcutaneous LD50 in mice: 253 mg/kg

[1]. Phosphorylation of histone H2AX is a powerful tool for detecting chemical photogenotoxicity. J Invest Dermatol. 2011 Jun;131(6):1313-21.

6-Methylcoumarin is a white crystalline solid with a vanilla-like odor and is insoluble in water. (NTP, 1992)
6-Methylcoumarin is a coumarin compound in which a methyl group is substituted at the 6-position hydrogen atom. It is a fragrance and an allergen.

---

Mechanism of Action
……6-Methylcoumarin……undergoes direct photolysis under mid-latitude sunlight at noon, with a half-life of approximately 83 minutes and a photolysis quantum yield of φ=3×10⁻³ at a wavelength of 313 nm. ……There is evidence that singlet oxygen (¹O₂) is generated in solutions containing 6-methylcoumarin. The quantum yield of ¹O₂ at a wavelength of 313 nm has been estimated to be φ=0.01. The generation of singlet oxygen (¹O₂) is significant because it is known to react with a variety of biomolecules, and its generation may at least partially contribute to the reported photosensitization and phototoxicity of 6-methylcytosine (6-MC). 4-Hydroxycoumarin derivatives and indanediones (also known as oral anticoagulants) are both vitamin K antagonists. Their use as rodenticides works by inhibiting vitamin K-dependent steps in the synthesis of various blood clotting factors. Vitamin K-dependent proteins in the coagulation cascade include procoagulant factors II (prothrombin), VII (prothrombin convertase), IX (Christmas factor), and X (Stuart-Proll factor), as well as coagulation inhibitory proteins C and S. All of these proteins are synthesized in the liver. Before being released into the bloodstream, various precursor proteins undergo extensive (intracellular) post-translational modifications. Vitamin K acts as a coenzyme in one modification process: the carboxylation of 10-12 glutamate residues at a specific site to generate γ-carboxyglutamate (Gla). The presence of these Gla residues is crucial for the procoagulant activity of various coagulation factors. Vitamin K hydroquinone (KH2) is the active coenzyme, which provides the energy required for the carboxylation reaction by oxidizing to vitamin K 2,3-epoxide (KO). Subsequently, this epoxide is recycled through two reduction steps catalyzed by KO reductase… KO reductase is the target of coumarin anticoagulants. Inhibition of KO reductase by coumarin anticoagulants leads to rapid depletion of KH2, effectively preventing the formation of Gla residues. This results in the accumulation of uncarboxylated coagulation factor precursors in the liver. In some cases, these precursor proteins are further processed without carboxylation and (depending on the species) may appear in the bloodstream. At this point, the uncarboxylated proteins are called decarboxylated coagulation factors. Normal coagulation factors circulate as prozymes and only participate in the coagulation cascade after activation through limited proteolytic degradation. Decarboxylation clotting factor lacks procoagulant activity (i.e., it cannot be activated) and cannot be converted into active proenzyme by the action of vitamin K. Although high levels of circulating decarboxylation clotting factor can be detected in humans receiving anticoagulation therapy, the levels of these factors are negligible in rats and mice treated with warfarin. /Anticoagulant rodenticide/

C10H8O2

160.1693

160.052

92-48-8

7092

White, crystalline solid
White needles from benzene

1.2±0.1 g/cm3

304.6±21.0 °C at 760 mmHg

73-76 °C(lit.)

124.3±19.5 °C

0.0±0.6 mmHg at 25°C

1.583

1.85

0

2

0

12

220

0

O1C(C([H])=C([H])C2C([H])=C(C([H])([H])[H])C([H])=C([H])C1=2)=O

FXFYOPQLGGEACP-UHFFFAOYSA-N

InChI=1S/C10H8O2/c1-7-2-4-9-8(6-7)3-5-10(11)12-9/h2-6H,1H3

6-methylchromen-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 : ~50 mg/mL (~312.17 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (15.61 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.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (15.61 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.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (15.61 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.

---

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