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Details

Stereochemistry ACHIRAL
Molecular Formula C12H8O4
Molecular Weight 216.1895
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of METHOXSALEN

SMILES

COC1=C2OC=CC2=CC3=C1OC(=O)C=C3

InChI

InChIKey=QXKHYNVANLEOEG-UHFFFAOYSA-N
InChI=1S/C12H8O4/c1-14-12-10-8(4-5-15-10)6-7-2-3-9(13)16-11(7)12/h2-6H,1H3

HIDE SMILES / InChI

Description

Methoxsalen — also called xanthotoxin, marketed under the trade names Oxsoralen, Deltasoralen, Meladinine — is a drug used to treat psoriasis, eczema, vitiligo, and some cutaneous lymphomas in conjunction with exposing the skin to UVA light from lamps or sunlight. Methoxsalen modifies the way skin cells receive the UVA radiation, allegedly clearing up the disease. The dosage comes in 10 mg tablets, which are taken in the amount of 30 mg 75 minutes before a PUVA (psoralen + UVA) light treatment. Chemically, methoxsalen belongs to a class of organic natural molecules known as furanocoumarins. They consist of coumarin annulated with furan. It can also be injected and used topically. The exact mechanism of action of methoxsalen with the epidermal melanocytes and keratinocytes is not known. The best known biochemical reaction of methoxsalen is with DNA. Methoxsalen, upon photoactivation, conjugates and forms covalent bonds with DNA which leads to the formation of both monofunctional (addition to a single strand of DNA) and bifunctional adducts (crosslinking of psoralen to both strands of DNA) Reactions with proteins have also been described. Methoxsalen acts as a photosensitizer. Administration of the drug and subsequent exposure to UVA can lead to cell injury. Orally administered methoxsalen reaches the skin via the blood and UVA penetrates well into the skin. If sufficient cell injury occurs in the skin, an inflammatory reaction occurs. The most obvious manifestation of this reaction is delayed erythema, which may not begin for several hours and peaks at 48–72 hours. The inflammation is followed, over several days to weeks, by repair which is manifested by increased melanization of the epidermis and thickening of the stratum corneum. The mechanisms of therapy are not known. In the treatment of vitiligo, it has been suggested that melanocytes in the hair follicle are stimulated to move up the follicle and to repopulate the epidermis. In the treatment of psoriasis, the mechanism is most often assumed to be DNA photodamage and resulting decrease in cell proliferation but other vascular, leukocyte, or cell regulatory mechanisms may also be playing some role. Psoriasis is a hyperproliferative disorder and other agents known to be therapeutic for psoriasis are known to inhibit DNA synthesis. The most commonly reported side effect of methoxsalen alone is nausea, which occurs with approximately 10% of all patients. This effect may be minimized or avoided by instructing the patient to take methoxsalen with milk or food, or to divide the dose into two portions, taken approximately one-half hour apart. Other effects include nervousness, insomnia, and psychological depression.

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
8-MOP
Primary
8-MOP
Palliative
8-MOP

Cmax

ValueDoseCo-administeredAnalytePopulation
129 ng/mL
0.6 mg/kg single, oral
METHOXSALEN plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
521 ng × h/mL
0.6 mg/kg single, oral
METHOXSALEN plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
2.38 h
0.6 mg/kg single, oral
METHOXSALEN plasma
Homo sapiens

Doses

AEs

Drug as perpetrator​

Drug as victim

Tox targets

PubMed

Sample Use Guides

In Vivo Use Guide
VITILIGO THERAPY : Two capsules (10 mg each) in one dose taken with milk or in food two to four hours before ultraviolet light exposure. PSORIASIS THERAPY: The methoxsalen capsules should be taken 2 hours before UVA exposure with some food or milk
Route of Administration: Oral
In Vitro Use Guide
8-Methoxypsoralen inhibited both the phytohemagglutinin and concanavalin A-induced proliferation of normal human peripheral blood lymphocytes in a time and dose-dependent manner.