ABCG2 (IC50 = 1.2 μM in HCT116/5-FU cells; Ki = 0.9 μM for ABCG2-mediated drug efflux inhibition) [1]
- Cytochrome P450 enzymes (CYP1A2, CYP2C9, CYP2D6, CYP3A4; inhibitory activity with IC50 values ranging from 3.5 to 12.8 μM) [2]
- Estrogen receptor α (ERα; binding affinity with Ki = 2.7 μM) [2]

Psoralen prevents rather than promotes apoptosis in MCF-7/ADR cell proliferation, as evidenced by G0/G1 phase arrest. Psoralen inhibits ATPase activity instead of decreasing P-gp expression to reverse MDR (multidrug resistance). Psoralen represses EMT, potentially by preventing NF-κB activation, which limits the migration potential of MCF-7/ADR cells. When longwave UV light activates pristralens, a class of photoactive compounds, DNA is easily alkylated. When MCF-7/ADR cells are exposed to low concentrations of psoralen (<10.75 µM) and high concentrations (>21.5 µM), their proliferation is markedly enhanced. Breast cancer metastases can be prevented by prisoralen. Numerous cell processes, such as migration, proliferation, inflammation, and death, are mediated by psoralen[1].

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In human colon cancer HCT116 and SNU-C5 cells, psoralen (0.5–4 μM) enhanced the antiproliferative activity of 5-fluorouracil (5-FU) by 2.3–4.1 folds. It downregulated ABCG2 mRNA and protein expression via inhibiting the PI3K/Akt signaling pathway, reducing 5-FU efflux and increasing intracellular 5-FU accumulation (intracellular 5-FU concentration increased by 38–62% at 2 μM psoralen) [1]
- Against Staphylococcus aureus and Escherichia coli, psoralen showed antibacterial activity with MIC values of 16 μg/mL and 32 μg/mL, respectively, by disrupting bacterial cell membrane integrity [2]
- In LPS-induced RAW264.7 macrophages, psoralen (1–10 μM) inhibited NO production (inhibition rate up to 78% at 10 μM) and reduced TNF-α, IL-6 mRNA expression via suppressing NF-κB activation [2]
- In MCF-7 breast cancer cells, psoralen (2–8 μM) induced G0/G1 cell cycle arrest and apoptosis (apoptosis rate of 23.5% at 8 μM) by regulating ERα-mediated signaling [2]

Psoralen has been identified as a tumor suppressor in a number of different tumors[1]. In both male and female mice, psoralen reduces osteoporosis brought on by a lack of sex hormone. By promoting osteoblastic differentiation from bone mesenchymal stem cells, it has an antiosteoporosis effect in rats with osteoporotic ovariectomy[2].

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In BALB/c nude mice bearing HCT116/5-FU xenografts, combined administration of psoralen (20 mg/kg, i.p., once daily) and 5-FU (10 mg/kg, i.p., once every 2 days) for 21 days significantly inhibited tumor growth (tumor volume inhibition rate of 67.2%) compared with 5-FU monotherapy (inhibition rate of 28.5%). No obvious body weight loss was observed in the combination group [1]
- In ovalbumin-induced allergic asthma mice, psoralen (5–20 mg/kg, p.o., once daily for 14 days) reduced airway hyperresponsiveness, eosinophil infiltration in lung tissues, and levels of IgE, IL-4, IL-13 in serum (IL-4 level decreased by 45% at 20 mg/kg) [2]

ABCG2 ATPase activity assay: Membrane vesicles containing human ABCG2 were incubated with psoralen (0.1–10 μM) and ATP. The amount of inorganic phosphate released was measured to evaluate ATPase activity. Psoralen stimulated ABCG2 ATPase activity with an EC50 of 1.5 μM, indicating direct binding to ABCG2 [1]
- CYP450 enzyme inhibition assay: Human liver microsomes were incubated with psoralen (0.1–50 μM) and specific substrates for CYP1A2, CYP2C9, CYP2D6, CYP3A4. The formation of metabolites was quantified by HPLC-MS/MS to calculate IC50 values for each CYP enzyme [2]
- ERα binding assay: Recombinant ERα protein was incubated with psoralen (0.1–20 μM) and [3H]-estradiol. The bound radioactivity was measured by scintillation counting to determine the binding affinity (Ki value) [2]

The MTT assay is used to measure the effects of psoralen on cell proliferation. MCF-10A and MCF-7/ADR cells are cultivated for 48 hours at a cell density of 2×10⁴ per well in 96-well plates. After that, the medium is taken out and replaced with new medium that has varying amounts of psoralen (0, 21.5, 43.0, 64.5, 86.0, and 107.5 μM) for 48 hours. The negative control group's cells are cultured in RPMI-1640 culture medium with 0.1% dimethyl sulfoxide (DMSO) added as a supplement. After incubating the cells for four hours with 10 µL MTT (5 mg/mL), the medium is discarded and 200 µL DMSO is added. After the crystals have completely dissolved, the spectrophotometric absorbance is measured at 490 nm using an enzyme-labeling apparatus.

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Cell viability assay: HCT116/SNU-C5 cells were seeded in 96-well plates (5×103 cells/well) and incubated for 24 h. Psoralen (0.1–8 μM) alone or with 5-FU (10 μM) was added, and cells were cultured for another 48 h. CCK-8 reagent was added, and absorbance at 450 nm was measured to calculate cell viability [1]
- Western blot analysis: HCT116 cells treated with psoralen (0.5–4 μM) for 48 h were lysed. Proteins were separated by SDS-PAGE, transferred to PVDF membranes, and probed with antibodies against ABCG2, PI3K, Akt, p-Akt. Band intensity was quantified using ImageJ software [1]
- Apoptosis assay: MCF-7 cells were treated with psoralen (2–8 μM) for 72 h. Cells were stained with Annexin V-FITC and propidium iodide, then analyzed by flow cytometry to determine apoptotic cell percentage [2]
- RT-PCR assay: RAW264.7 macrophages treated with psoralen (1–10 μM) and LPS (1 μg/mL) for 24 h were used for total RNA extraction. cDNA was synthesized, and PCR was performed with primers for TNF-α, IL-6, NF-κB p65 to quantify mRNA expression [2]

ICR mice
10 mg/kg and 20 mg/kg
intragastrically

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Xenograft tumor model: BALB/c nude mice (6–8 weeks old, male) were subcutaneously injected with HCT116/5-FU cells (5×106 cells/mouse) into the right flank. When tumors reached 100 mm3, mice were randomly divided into 4 groups (n=6): control (saline), psoralen alone (20 mg/kg, dissolved in 10% DMSO + 90% saline), 5-FU alone (10 mg/kg), and combination group. Psoralen was administered intraperitoneally once daily, and 5-FU was administered intraperitoneally once every 2 days for 21 days. Tumor volume and body weight were measured every 3 days [1]
- Allergic asthma model: BALB/c mice (6–8 weeks old, female) were sensitized with ovalbumin (OVA) + aluminum hydroxide on days 0 and 14. From day 21 to 27, mice were challenged with OVA aerosol. Psoralen (5, 10, 20 mg/kg) was dissolved in 0.5% carboxymethylcellulose sodium and administered orally once daily from day 18 to 27. On day 28, mice were sacrificed for sample collection [2]

Absorption, Distribution and Excretion
Objective: To investigate the nasal absorption patterns of psoralen and isopsoralen at different concentrations. Methods: An in situ nasal circulation model was established in rats, and the contents of psoralen and isopsoralen were determined by high-performance liquid chromatography (HPLC). Results: The nasal absorption of psoralen and isopsoralen followed zero-order kinetics and reached saturation with increasing concentration. Conclusion: Appropriate concentrations are required for the preparation of nasal psoralen and isopsoralen. Metabolism/Metabolites Known human metabolites of psoralen include 5,7,11-trioxatetracyclo[8.4.0.03,8.04,6]tetradecano-1,3(8),9,13-tetraen-12-one. Absorption: After oral administration of psoralen (50 mg/kg) to rats, the maximum plasma concentration (Cmax) was 1.8 μg/mL, and the time to peak concentration (Tmax) was 1.5 h. The oral bioavailability was 32.6% [2]
- Distribution: Psoralen is widely distributed in rat tissues. Two hours after oral administration, the highest concentrations were found in the liver (3.2 μg/g) and kidneys (2.7 μg/g) [2]
- Metabolism: Psoralen is mainly metabolized in human liver microsomes via CYP3A4 and CYP1A2 to generate hydroxylated metabolites (5-hydroxypsoralen and 8-hydroxypsoralen) [2]
- Excretion: Within 72 hours after oral administration to rats, 68.3% of psoralen was excreted in feces and 12.5% in urine, mainly in the form of metabolites [2]
- Half-life: The elimination half-life (t1/2) of psoralen after oral administration to rats was 4.2 hours [2]

Toxicity Summary
Identification and Uses: Psoralen is a solid. Psoralen photochemotherapy (PUVA) combines a photosensitizing drug (psoralen) with UVA radiation for the treatment of skin diseases. The introduction of PUVA therapy can be considered one of the most significant advances in dermatology over the past 30 years. Human Studies: Receiving more than 350 PUVA treatments significantly increases the risk of squamous cell carcinoma. Receiving fewer than 150 PUVA treatments has at most a minor effect on the risk of squamous cell carcinoma. Even high-dose PUVA treatment does not significantly increase the risk of basal cell carcinoma. When assessing the risks of this therapy relative to other treatments for severe psoriasis, the risk of squamous cell carcinoma in patients receiving long-term PUVA treatment should be considered. Psoralen UVB radiation (PUVB) may cause blue spot vitiligo. Psoralen can produce a very unique type of DNA damage called interstrand crosslinks (ICLs). ICLs can severely impair DNA replication and transcription and lead to programmed cell death. Studies have shown that PUVA therapy is more conducive to the formation of psoralen photooxidation products, which have immunosuppressive effects rather than membrane-damaging effects. In vitro experiments have shown that psoralen can inhibit the activity of normal human hepatocytes L02 by inducing S-phase arrest. In addition, psoralen can upregulate the protein levels of cyclin E1 and p27 in these cells. Animal experiments: Mice were administered 400 mg/kg or 800 mg/kg of psoralen orally by gavage and sacrificed 24 hours later. Changes in various hepatotoxicity indicators showed that psoralen can cause mild liver injury in mice. In addition, psoralen can upregulate the protein levels of cyclin E1 and p27 in mouse liver. In rats, the liver is the target organ of psoralen toxicity. Multivariate analysis identified 7 metabolites in serum samples and 15 metabolites in liver samples as potential biomarkers of psoralen-induced liver injury. In addition, psoralen can cause amino acid metabolism disorders, especially affecting the biosynthesis of valine, leucine, and isoleucine in both serum and liver samples. The mutagenic activity of psoralen was investigated using the HGPRT system in V79 Chinese hamster cells cultured in vitro. Psoralen effectively induced HGPRT mutants upon activation by near-ultraviolet (NUV). Albino guinea pigs were irradiated with furanocoumarin derivatives in combination with 320-400 nm ultraviolet light, and DNA was extracted from their epidermis. Electron microscopy was sensitive enough to determine the upper limit of one crosslink per 10 × 6 nucleotide pairs (80 crosslinks per chromosome) in low-dose studies. In vitro experiments showed that psoralen inhibited monoamine oxidase (MAO) activity in rat brain mitochondria, with a stronger inhibitory effect on MAO-A activity than on MAO-B activity. Ecotoxicity studies revealed a distinct bimodal distribution of psoralen crosslinks in fungal, plant, and animal rRNA genes, suggesting that these genes may largely lack nucleosomes during active transcription. Researchers also studied the chromatin structure of multicopy rRNA and histone genes during early sea urchin embryonic development. The results showed that psoralen crosslinking of low-expression rRNA genes exhibited a unimodal distribution and a low degree of crosslinking, which was distinctly different from the situation in all other studied organisms. Early histone genes were more easily crosslinked by psoralen in the active state than in the inactive state. Many furanocoumarins act based on their ability to form photoadducts with DNA and other cellular components, such as RNA, proteins, and membrane proteins, including phospholipases A2 and C, calcium-dependent and cAMP-dependent protein kinases, and epidermal growth factor. Furanocoumarins insert between DNA base pairs and generate cycloadducts upon UVA irradiation (L579). Hepatotoxicity: In open-label trials, 2% to 12% of subjects receiving methoxsalen and UVA therapy experienced elevated serum ALT or AST levels. These elevations were typically mild to moderate, asymptomatic, and self-limiting. There have also been reports of clinically significant acute liver injury with oral methoxsalen treatment, but these are limited to case reports, one of which was attributed to topical methoxsalen treatment. The onset time is 1 to 5 months, with a typical incubation period of 6 to 8 weeks. The onset is usually insidious, beginning with nausea and abdominal pain, followed by jaundice. Fever is present in some cases, but rash and eosinophilia are uncommon. The typical pattern of liver injury is hepatocellular. Most published cases of psoralen hepatotoxicity are mild to moderate, but there are also reports of severe acute liver injury in patients with pre-existing cirrhosis who ultimately died from liver failure after taking methoxsalen. Most cases resolve within 6 to 8 weeks. Psoralen is also present in many herbal products used to treat a variety of conditions, including psoriasis and vitiligo. There have been reports of acute liver injury from the use of Psoralea corylifolia seeds, powder, and tea (with various Chinese names such as Psoralea tea, Xinbugansu, and Qubai Babu tablets). Chemical analysis has shown that these products contain psoralen. These cases exhibit clinical characteristics similar to methoxsalen poisoning, with an incubation period of 1 to 2 months, presenting with a hepatocellular injury pattern, without immune hypersensitivity or autoimmune features, and a self-limiting course, recovering within 6 to 8 weeks.
Probability Score: C (Possibly a rare cause of clinically significant liver injury)
Interaction

Background: The use of psoralen combined with UVA (PUVA) therapy in patients with type I to II photosensitive skin is limited by acute phototoxic side effects and potential long-term carcinogenicity. Objective: This study aimed to evaluate, from clinical and histological perspectives, the effect of oral Plopodium leucotomos (PL) extract on reducing PUVA-induced phototoxicity in humans. Methods: Ten healthy subjects with photosensitive skin types II to III were included, receiving either PUVA therapy (oral 8-methoxypsoralen 0.6 mg/kg) or PUVA combined with oral PL (7.5 mg/kg). Results: Clinically, the phototoxicity of the skin in the PL treatment group was consistently lower than that in the control group from 48 to 72 hours (P<0.005), and pigmentation was also significantly reduced after 4 months. Histologically, the number of sunburned cells in the skin of the PL treatment group was significantly reduced (P=0.05), the number of Langerhans cells was preserved (P≤0.01), trypsin-positive mast cell infiltration was reduced (P<0.05), and vasodilation was decreased (P≤0.01). No difference was observed in Ki-67+ proliferating cells. Conclusion: PL is an effective chemopreservative that can counteract PUVA-induced skin phototoxicity and significantly protect the skin from PUVA damage, as confirmed by histological results. Chemotherapy is a recommended treatment for advanced cancer. However, the emergence of multidrug resistance (MDR), the ability of cancer cells to develop resistance to multiple drugs simultaneously, limits the efficacy of chemotherapy. Previous studies have shown that herbal or natural foods may serve as effective chemopreventive agents for various cancers. This study aimed to investigate the ability of psoralen to reverse multidrug resistance in docetaxel (DOC)-resistant A549 cells (A549/D16) and its potential mechanism. Our results showed that psoralen combined with docetaxel (DOC) treatment reduced the viability of the A549/D16 subline, while psoralen had no effect on the proliferation of A549 and A549/D16 cells. Furthermore, psoralen treatment reduced the mRNA and protein levels of ABCB1, and flow cytometry analysis confirmed the decrease in ABCB1 activity. Based on these results, we believe that psoralen may reverse multidrug resistance by inhibiting the expression of the ABCB1 gene and protein. This inhibition leads to reduced ABCB1 activity and decreased efflux of anticancer drugs, ultimately reversing resistance and thus making resistant cells more sensitive to chemotherapy drugs when used in combination. Psoralen (PRN), a furanocoumarin compound, is a major active ingredient in herbal plants. PRN has been used in China to treat various skin diseases. We evaluated the inhibitory effect of PRN on cytochrome P450 2B6 (CYP2B6) and found that PRN induced time-, concentration-, and NADPH-dependent inactivation of CYP2B6, with KI and kinact values of 110.2 μM and 0.200 min⁻¹, respectively. The CYP2B6 substrate ticlopidine prevented PRN-induced enzyme inactivation. The exogenous nucleophiles glutathione (GSH) and catalase/superoxide dismutase had limited protective effects on CYP2B6. The estimated inactivation partition ratio was approximately 400. GSH capture assays showed the formation of epoxides and/or γ-ketoenal intermediates during microsomal incubation with PRN. In conclusion, PRN was demonstrated to be a mechanism-based inhibitor of CYP2B6.
Naturally occurring furanocoumarin compounds psoralen (PRN) and isopsoralen (IPRN) are bioactive components in herbal plants and are widely used as active ingredients in various traditional Chinese medicines. This study investigated the inhibitory effects of PRN and IPRN on CYP1A2 in vitro, in vivo (rat), and in human liver microsomes. The results showed that both compounds exhibited reversible and time-dependent inhibitory effects on rat microsomal CYP1A2. The IC50, kinact, and KI values for PRN were 10.4 ± 1.4 μM, 0.060 ± 0.002 min⁻¹, and 1.13 ± 0.12 μM, respectively, while the corresponding values for IPRN were 7.1 ± 0.6 μM, 0.10 ± 0.01 min⁻¹, and 1.95 ± 0.31 μM, respectively. In human liver microsome incubation experiments, both compounds exhibited potent and reversible CYP1A2 inhibition, with IC50 values of 0.26 ± 0.01 μM and 0.22 ± 0.03 μM for PRN and IPRN, respectively. However, time-dependent inhibition was observed only in IPRN, with kinact and KI values of 0.050 ± 0.002 min⁻¹ and 0.40 ± 0.06 μM, respectively. Combined administration of PRN or IPRN significantly inhibited CYP1A2 activity in rats, increasing the area under the curve (AUC) of phenacetin by more than 5-fold. Simcyp simulations predicted that PRN would increase the AUC of phenacetin by 1.71-fold and 2.12-fold in healthy volunteers and smokers, respectively. IPRN, on the other hand, would increase the AUC of phenacetin by 3.24-fold and 5.01-fold in healthy volunteers and smokers, respectively. These findings are the first report to provide a detailed comparison of the potential drug interactions between psoralen (PRN) and isopsoralen (IPRN), and provide useful information for balancing safe and effective doses of PRN and IPRN. For more complete data on psoralen interactions (40 in total), please visit the HSDB record page. Phototoxicity: Psoralen (10–50 μM) induced phototoxicity in HaCaT keratinocytes upon exposure to UVA radiation (365 nm, 2 J/cm2), resulting in a 35–70% decrease in cell viability [2]. Hepatotoxicity: High doses of psoralen (100 mg/kg, orally, once daily for 28 days) in rats resulted in a slight increase in serum ALT and AST levels (1.5–2.0 times that of the control group), but no significant histological changes were observed in liver tissue [2]. Plasma protein binding: The plasma protein binding rate of psoralen was 82.3%. Protein binding in human plasma [2] - No significant acute toxicity was observed in mice after oral administration of psoralen at 200 mg/kg (LD50 > 200 mg/kg, oral) [2]

[1]. Biol Pharm Bull . 2016 May 1;39(5):815-22.

[2]. BioMed Research International. 2016, 2016:6869452.

Psoralen is the simplest member of the psoralen class of compounds, with the chemical formula 7H-furano[3,2-g]chromene, containing a ketone group at the 7-position. It is found in plants such as Psoralea corylifolia and Ficus salicifolia, and is a plant metabolite. 8-Methoxysarin and 5-methoxysarin are furanocoumarins, collectively known as psoralens, which possess photosensitizing activity and can be taken orally or topically, often in combination with ultraviolet radiation for the treatment of psoriasis and vitiligo. Psoralen is associated with a low incidence of transient elevations in serum enzymes during treatment and rare cases of clinically significant acute liver injury. Psoralen has been reported in Ficus erecta var., including Beecheyana, Hoita macrostachya, and other organisms with relevant data. Psoralen is a furanocoumarin that can intercalate into DNA, inhibiting DNA synthesis and cell division. Psoralen is used in photochemotherapy with high-intensity long-wave UVA irradiation. Psoralen is a tricyclic furanocoumarin with a strong tendency to intercalate into DNA base pairs. In the presence of psoralen, irradiation of nucleic acids with long-wave ultraviolet light (~360 nm) causes a 2+2 cycloaddition reaction between one of its two photoreactive sites and the 5,6-carbon bond of a pyrimidine, resulting in double-stranded nucleic acid cross-linking. Carrots contain psoralen. Psoralen is found in common vegetables such as parsnip and celery, especially in diseased or "rotten" vegetables. Psoralen is an important mutagen and is frequently used in molecular biology research. Studies have shown that psoralen has anti-proliferative, anti-allergic, and antihistamine functions (A7781, A7782, A7782). Psoralen belongs to the furanocoumarin class of compounds. These compounds are polycyclic aromatic compounds whose structure includes a furan ring partially fused with a coumarin.
A naturally occurring furanocoumarin found in plants of the genus Psoralea. Upon activation by ultraviolet light, it can bind to DNA through single-strand and double-strand cross-links.
See also: Angelica sinensis (part). Boswellia caronii fruit (part).

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Therapeutic Uses
/EXPL THER/ Osteoporosis is a systemic skeletal disease characterized by the systematic destruction of bone mass and microstructure. With improved living standards, the treatment of osteoporosis is receiving increasing attention. This study aimed to verify the osteoprotective effects of psoralen and isopsoralen on male and female mice. Male and female mice were divided into 7 groups: control group (sham-operated group), model group (oophorectomy or orchiectomy), positive control group (female mice given estradiol valerate; male mice given alendronate sodium), psoralen group (10 mg/kg and 20 mg/kg), and isopsoralen group (10 mg/kg and 20 mg/kg). After 8 weeks of administration of psoralen and isopsoralen, osteoporosis improved, with CT scans and pathological results showing increased bone strength and improved trabecular microstructure. Serum alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRACP), osteocalcin (OC), and type I collagen C-terminal cross-linked peptide (CTX-1) were measured. Decreased TRACP and increased ALP/TRACP suggested bone repair. These results indicate that psoralen and isopsoralen may serve as promising natural compounds for the treatment of osteoporosis in both men and women.
/EXPL THER/ This study explores X-PACT (X-ray psoralen-activated cancer therapy): a novel approach for treating solid tumors. X-PACT utilizes psoralen, a potent anticancer drug currently used in extracorporeal phototherapy (ECP) for proliferative diseases and cutaneous T-cell lymphomas. It has been reported that photoactivated psoralen possesses immunogenicity, which may contribute to long-term clinical efficacy. Because psoralen requires UVA light activation, and UVA light has limited penetration into tissues, psoralen therapy has been limited to superficial or in vitro applications to date. X-PACT overcomes this challenge by activating psoralen with UV light released from novel unbound phosphors (co-incubated with psoralen). These phosphors absorb X-rays and re-emit at UV wavelengths (phosphorescence). The efficacy of X-PACT has been evaluated in vitro and in vivo. In vitro studies used breast cancer (4T1), glioma (CT2A), and sarcoma (KP-B) cell lines. Cells were treated with X-PACT, with variations in drug (psoralen and phosphorus) concentrations and radiation parameters (energy, dose, and dose rate). Efficacy was primarily assessed using flow cytometry combined with other auxiliary assays and in vivo mouse experiments. In vitro studies showed that, unlike psoralen or phosphorus alone, X-PACT significantly induced tumor cell apoptosis and cytotoxicity (p<0.0001). We also found that apoptosis increased with increasing phosphorus, psoralen, or radiation doses. Finally, in preliminary in vivo studies of BALB/c mouse 4T1 tumors, we found that X-PACT significantly slowed tumor growth compared to saline or AMT+X-rays (p<0.0001). In conclusion, these studies demonstrate the potential therapeutic efficacy of X-PACT and lay the foundation and theoretical basis for future research. In summary, X-PACT represents a novel therapeutic approach that delivers well-tolerated low-dose X-ray radiation to specific tumor sites to generate UVA light, thereby activating the short-term and potentially long-term antitumor activity of photosensitizing therapies such as psoralen.
/EXPL THER/ Mycosis fungoides with large cell transformation has historically had a poor prognosis. Cases of mycosis fungoides with large cell transformation in children are rare, with only three reported in the literature. We report the first case of a child achieving near-complete remission of mycosis fungoides with large cell transformation after receiving psoralen combined with UVA, interferon-α, and local radiation therapy.
/EXPL THER/ Background: Isotretinoin has been used in combination with oral psoralen and UVA (PUVA) and narrow-band UVB (NBUVB) for the treatment of psoriasis, particularly in women of childbearing age. The efficacy of oral psoralen combined with solar irradiation (PUVAsol) is comparable to PUVA therapy. This study aimed to compare the efficacy of oral PUVAsol versus oral isotretinoin combined with PUVAsol in the treatment of patients with chronic plaque psoriasis. Methods: Forty patients with psoriasis vulgaris were randomly assigned to two groups. Group A (control group) received PUVAsol alone. Group B (intervention group) received PUVAsol combined with isotretinoin (0.5 mg/kg/day). Psoriasis Area and Severity Index (PASI) scores were recorded at baseline and at weeks 4, 8, and 12 after treatment. The Dermatology Life Quality Index (DLQI) was assessed at baseline and at week 12 post-treatment. The study endpoint was PASI 75 or 12 weeks of treatment, whichever came first. Results: 35 patients completed the study. There were statistically significant differences between the two groups in the number of patients achieving the PASI 75 endpoint, PASI score at the end of 12 weeks, mean duration of PASI 75, number of PUVAsol treatment cycles required to achieve PASI 75, and mean cumulative dose of 8-methoxypsoralen required to achieve PASI 75. Conclusion: Isotretinoin in combination with PUVAsol is more effective than PUVAsol alone in treating chronic plaque psoriasis.
For more complete data on the therapeutic uses of psoralen (14 types), please visit the HSDB records page.

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Drug Warning
This study aims to raise awareness of the potential risks of unexpected adverse reactions from photochemotherapy (psoralen-UVA or PUVA), which is used to treat certain skin conditions and commercially for cosmetic tanning. In addition to common PUVA side effects such as erythema and itching, unexpected adverse reactions, such as extensive burns, occasionally occur. Our observations indicate that 6 of these were due to medical staff error, and another 6 were due to improper patient operation under unsupervised conditions. Cases requiring photochemotherapy included 7 cases of vitiligo, 3 cases of psoriasis, and 2 cases of tanning. Accidental excessive UV radiation doses were approximately 3–10 times the empirically normal dose. We had 5 patients who should have received topical PUVA treatment but instead received oral PUVA doses. One patient received oral PUVA treatment with 5-methoxypsoralen (5-MOP) tablets while also using 8-methoxypsoralen (8-MOP) cream. Three other patients tanned within 1–3 hours after PUVA treatment.
A young couple opted for 5-MOP to enhance tanning and tanned approximately one hour later. Another patient restarted PUVA therapy six months after discontinuation, but at the previous dose instead of the starting dose. All cases developed erythema and blisters of second-degree burns 36–72 hours after PUVA treatment, affecting 5–25% of the body surface area. Of the 12 patients, 3 were hospitalized and 9 were treated as outpatients. All patients recovered within 1–3 weeks without skin grafting and without significant sequelae other than post-inflammatory hyperpigmentation. Potential adverse effects on the fetus: No animal studies have been conducted. Effects on humans are unknown. Use only when clearly needed. Potential side effects on breastfed infants: It is unclear whether they are excreted. Use should be avoided. FDA Classification: C (C = Laboratory animal studies have shown adverse effects on the fetus (teratogenicity, embryonic lethality, etc.), but there are no controlled studies in pregnant women. Despite the potential risks, the benefits of using this drug in pregnant women may be acceptable, or there are no adequate laboratory animal studies or studies in pregnant women.) /Psoralen/ /Excerpt from Table II/
Psoralen combined with ultraviolet A irradiation (PUVA therapy) is commonly used to treat vitiligo, with a common efficacy being perifollicular pigment regeneration. However, overuse of PUVA therapy may lead to adverse reactions. We report a case of a patient with generalized vitiligo who had received extensive topical and systemic PUVA therapy for many years, subsequently developing large areas of stellate and irregularly shaped black and brown macules (freckles). Interestingly, freckles appeared not only in normally pigmented skin but also in depigmented lesions lacking the perifollicular reaction pattern. Lesions occurred in both exposed and unexposed areas of skin. No evidence of cutaneous malignancy was observed clinically, and no melanocyte atypia was detected histopathologically. Cryotherapy can be used to treat freckles; however, it was not applicable in this case due to the large extent of the lesions. Background: Patients receiving psoralen and UVA (PUVA) treatment may develop changes in skin appearance, including actinic degeneration and pigmentation changes. Objective: Our aim was to quantify the extent and risk factors for the progression of actinic degeneration and pigmentation changes in patients receiving PUVA treatment. Methods: Based on standardized dermatological examinations of patients enrolled in follow-up studies of PUVA in 1977 and 1998, we assessed the prevalence and degree of change of actinic degeneration and pigmentation abnormalities in the hands and buttocks. Results: From 1977 to 1998, the prevalence of moderate to severe actinic degeneration in the hands increased from 15.6% to 60.5%, and in the buttocks from 2.2% to 21.3%. During the same period, the prevalence of corresponding degrees of pigmentation changes in the hands increased from 15.6% to 58.6%, and in the buttocks from 12.6% to 24.7%. The extent of PUVA treatment was the strongest predictor of an increase in the clinical degree of actinic degeneration or pigmentation changes. Conclusion: Long-term PUVA treatment is associated with a persistent increase in actinic degeneration and pigmentation abnormalities of the skin, whether in areas normally exposed to sunlight or in areas not exposed to sunlight.
For more drug warnings (complete) data on psoralen (of 8), please visit the HSDB record page.

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Psoralen is a natural furanocoumarin compound isolated from plants of the Apiaceae and Leguminosae families[2].
- The combination of psoralen and 5-fluorouracil (5-FU) provides a potential therapeutic strategy for 5-FU-resistant colon cancer by targeting ABCG2-mediated multidrug resistance[1].
-Psoralen has a variety of pharmacological activities, including antitumor, antibacterial, anti-inflammatory, immunomodulatory, and estrogen-like effects[2].

C11H6O3

186.16

186.031

66-97-7

6199

White to off-white solid powder

1.4±0.1 g/cm3

362.6±27.0 °C at 760 mmHg

160-162 °C

173.1±23.7 °C

0.0±0.8 mmHg at 25°C

1.667

1.67

0

3

0

14

284

0

ZCCUUQDIBDJBTK-UHFFFAOYSA-N

InChI=1S/C11H6O3/c12-11-2-1-7-5-8-3-4-13-9(8)6-10(7)14-11/h1-6H

furo[3,2-g]chromen-7-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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (13.43 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 (13.43 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
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 (13.43 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.)