Psoromic acid
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Enzyme inhibitors |
| Catalog number | BBF-05693 |
| CAS | 7299-11-8 |
| Molecular Weight | 358.30 |
| Molecular Formula | C18H14O8 |
| Purity | ≥95% |
Online Inquiry
Description
Psoromic acid is a selective inhibitor of Rab geranylgeranyl transferase and P. falciparum fatty acid synthesis (FAS) II enzymes.
Specification
| Synonyms | 10-formyl-9-hydroxy-3-methoxy-4,7-dimethyl-6-oxobenzo[b][1,4]benzodioxepine-1-carboxylic acid; NSC 92186; Parellic Acid; Psoromsaeure; Sulcatic acid; Sqamaric |
| Storage | Store at -20°C |
| IUPAC Name | 4-Formyl-3-hydroxy-8-methoxy-1,9-dimethyl-11-oxo-11H-dibenzo[b,e][1,4]dioxepin-6-carboxylic Acid |
| Canonical SMILES | CC1=CC(=C(C2=C1C(=O)OC3=C(O2)C(=CC(=C3C)OC)C(=O)O)C=O)O |
| InChI | InChI=1S/C18H14O8/c1-7-4-11(20)10(6-19)15-13(7)18(23)26-14-8(2)12(24-3)5-9(17(21)22)16(14)25-15/h4-6,20H,1-3H3,(H,21,22) |
| InChI Key | FUCWJKJZOHOLEO-UHFFFAOYSA-N |
Properties
| Appearance | Solid |
| Boiling Point | 641.7°C at 760 mmHg |
| Melting Point | 265-266°C |
| Density | 1.483 g/cm3 |
| Solubility | Soluble in DMSO, Ethanol |
Reference Reading
1. Psoromic Acid, a Lichen-Derived Molecule, Inhibits the Replication of HSV-1 and HSV-2, and Inactivates HSV-1 DNA Polymerase: Shedding Light on Antiherpetic Properties
Kateřina Berchová-Bímová, Javier Echeverría, Karel Šmejkal, Sherif T S Hassan, Miroslava Šudomová Molecules . 2019 Aug 11;24(16):2912. doi: 10.3390/molecules24162912.
Psoromic acid (PA), a bioactive lichen-derived compound, was investigated for its inhibitory properties against herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), along with the inhibitory effect on HSV-1 DNA polymerase, which is a key enzyme that plays an essential role in HSV-1 replication cycle. PA was found to notably inhibit HSV-1 replication (50% inhibitory concentration (IC50): 1.9 μM; selectivity index (SI): 163.2) compared with the standard drug acyclovir (ACV) (IC50: 2.6 μM; SI: 119.2). The combination of PA with ACV has led to potent inhibitory activity against HSV-1 replication (IC50: 1.1 µM; SI: 281.8) compared with that of ACV. Moreover, PA displayed equivalent inhibitory action against HSV-2 replication (50% effective concentration (EC50): 2.7 μM; SI: 114.8) compared with that of ACV (EC50: 2.8 μM; SI: 110.7). The inhibition potency of PA in combination with ACV against HSV-2 replication was also detected (EC50: 1.8 µM; SI: 172.2). Further, PA was observed to effectively inhibit HSV-1 DNA polymerase (as a non-nucleoside inhibitor) with respect to dTTP incorporation in a competitive inhibition mode (half maximal inhibitory concentration (IC50): 0.7 μM; inhibition constant (Ki): 0.3 μM) compared with reference drugs aphidicolin (IC50: 0.8 μM;Ki: 0.4 μM) and ACV triphosphate (ACV-TP) (IC50: 0.9 μM;Ki: 0.5 μM). It is noteworthy that the mechanism by which PA-induced anti-HSV-1 activity was related to its inhibitory action against HSV-1 DNA polymerase. Furthermore, the outcomes of in vitro experiments were authenticated using molecular docking analyses, as the molecular interactions of PA with the active sites of HSV-1 DNA polymerase and HSV-2 protease (an essential enzyme required for HSV-2 replication) were revealed. Since this is a first report on the above-mentioned properties, we can conclude that PA might be a future drug for the treatment of HSV infections as well as a promising lead molecule for further anti-HSV drug design.
2. Potential of lichen secondary metabolites against Plasmodium liver stage parasites with FAS-II as the potential target
Hua Xu, Peter J Tonge, Remo Perozzo, Duc-Hung Pham, Mire Zloh, Xujie Zhang, Christopher Stairiker, Deniz Tasdemir, Alice Tarun, Livia Vivas, Alexander D Crawford, Louis Maes, Camila V Esguerra, Scott G Franzblau, Ina L Lauinger J Nat Prod . 2013 Jun 28;76(6):1064-70. doi: 10.1021/np400083k.
Chemicals targeting the liver stage (LS) of the malaria parasite are useful for causal prophylaxis of malaria. In this study, four lichen metabolites, evernic acid (1), vulpic acid (2), psoromic acid (3), and (+)-usnic acid (4), were evaluated against LS parasites of Plasmodium berghei. Inhibition of P. falciparum blood stage (BS) parasites was also assessed to determine stage specificity. Compound 4 displayed the highest LS activity and stage specificity (LS IC50 value 2.3 μM, BS IC50 value 47.3 μM). The compounds 1-3 inhibited one or more enzymes (PfFabI, PfFabG, and PfFabZ) from the plasmodial fatty acid biosynthesis (FAS-II) pathway, a potential drug target for LS activity. To determine species specificity and to clarify the mechanism of reported antibacterial effects, 1-4 were also evaluated against FabI homologues and whole cells of various pathogens (S. aureus, E. coli, M. tuberculosis). Molecular modeling studies suggest that lichen acids act indirectly via binding to allosteric sites on the protein surface of the FAS-II enzymes. Potential toxicity of compounds was assessed in human hepatocyte and cancer cells (in vitro) as well as in a zebrafish model (in vivo). This study indicates the therapeutic and prophylactic potential of lichen metabolites as antibacterial and antiplasmodial agents.
3. Antimycobacterial, Enzyme Inhibition, and Molecular Interaction Studies of Psoromic Acid in Mycobacterium tuberculosis: Efficacy and Safety Investigations
Shanmugaraj Gowrishankar, Kateřina Berchová-Bímová, Sherif T S Hassan, Kannan R R Rengasamy, Miroslava Šudomová J Clin Med . 2018 Aug 20;7(8):226. doi: 10.3390/jcm7080226.
The current study explores the antimycobacterial efficacy of lichen-derived psoromic acid (PA) against clinical strains ofMycobacterium tuberculosis(M.tb). Additionally, the inhibitory efficacy of PA against two critical enzymes associated with M.tb, namely, UDP-galactopyranose mutase (UGM) and arylamine-N-acetyltransferase (TBNAT), as drug targets for antituberculosis therapy were determined. PA showed a profound inhibitory effect towards all the M.tb strains tested, with minimum inhibitory concentrations (MICs) ranging between 3.2 and 4.1 µM, and selectivity indices (SIs) ranging between 18.3 and 23.4. On the other hand, the standard drug isoniazid (INH) displayed comparably high MIC values (varying from 5.4 to 5.8 µM) as well as low SI values (13.0⁻13.9). Interestingly, PA did not exhibit any cytotoxic effects on a human liver hepatocellular carcinoma cell line even at the highest concentration tested (75 µM). PA demonstrated remarkable suppressing propensity against UGM compared to standard uridine-5'-diphosphate (UDP), with 85.8 and 99.3% of inhibition, respectively. In addition, PA also exerted phenomenal inhibitory efficacy (half maximal inhibitory concentration (IC50) value = 8.7 µM, and 77.4% inhibition) against TBNAT compared with standard INH (IC50value = 6.2 µM and 96.3% inhibition). Furthermore, in silico analysis validated the outcomes of in vitro assays, as the molecular interactions of PA with the active sites of UGM and TBNAT were unveiled using molecular docking and structure⁻activity relationship studies. Concomitantly, our findings present PA as an effective and safe natural drug plausible for use in controlling tuberculosis infections.
Recommended Products
| BBF-00677 | 3-Amino-3-deoxy-D-glucose | Inquiry |
| BBF-00764 | Cerebroside C | Inquiry |
| BBF-02642 | Lactonamycin | Inquiry |
| BBF-03753 | Baicalin | Inquiry |
| BBF-05862 | Epirubicin | Inquiry |
| BBF-01829 | Deoxynojirimycin | Inquiry |
Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
