 | |
| Names | |
|---|---|
| IUPAC name Solanid-5-en-3β-ol | |
| Systematic IUPAC name (2S,4aR,4bS,6aS,6bR,7S,7aR,10S,12aS,13aS,13bS)-4a,6a,7,10-Tetramethyl-2,3,4,4a,4b,5,6,6a,6b,7,7a,8,9,10,11,12a,13,13a,13b,14-icosahydro-1H-naphtho[2′,1′:4,5]indeno[1,2-b]indolizin-2-ol | |
| Other names Solatubin; Solatubine | |
| Identifiers | |
| |
3D model (JSmol) | |
| 45370 | |
| ChEBI | |
| ChEMBL | |
| ChemSpider | |
| ECHA InfoCard | 100.001.191 |
| EC Number |
|
| KEGG | |
| UNII | |
| |
| |
| Properties | |
| C27H43NO | |
| Molar mass | 397.647 g·mol−1 |
| Hazards[1] | |
| GHS labelling: | |
 | |
| Warning | |
| H302,H413 | |
| P264,P270,P273,P301+P312,P330,P501 | |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Solanidine is apoisonoussteroidal alkaloidchemicalcompound that occurs in plants of the familySolanaceae, such aspotato andSolanum americanum.[2][3] The sugar portion of glycoalkaloidshydrolyses in the body, leaving the solanidine portion.[4]
Solanidine is the hydrolyzed form[4] of several naturally occurring compounds all found in the Solanaceae family, such asglycoalkaloids,α-solanine andα-chaconine.[5][4] Solanidine is not commonly found in nature, but precursors to it are. Glycoalkaloids are one of the toxins present inSolanum dulcamara and can be found in otherSolanum plants as well such as potatoes, tomatoes and eggplant. Solanine is also found in all parts of the Solanum family species and is considered part of the plant's natural defenses. Chaconine is found in specifically green tubers and gives them their bitter taste. Solanidine is found naturally occurring in green potatoes and in theSolanum americanum[2][3] species. The theorized biosynthetic route for the creation of Solanidine proposed in 1977 within the Solanaceae family was thought to be derived fromcholesterol to the SA aglycone. This pathway was overturned in 2013 when a set of glycoalkaloid metabolism genes was found present in Solanaceae plants that participate in a SGA biosynthesis pathway.[6][7]
Solanidine occurs in theblood serum of normal healthy people who eat potato, and serum solanidine levels fall markedly once potato consumption ceases.[8] Solanidine from food is also stored in the human body for prolonged periods of time, and it has been suggested that it could be released during times of metabolic stress with the potential for deleterious consequences.[9] Solanidine is responsible forneuromuscular syndromes viacholinesterase inhibition.[10][11] Symptoms of cholinesterase inhibition includeinsomnia, nausea and vomiting, accidental injury, headache, dizziness,bradycardia,hypotension,ecchymosis, and sleep disturbance.[12] Solanidine poisoning is rarely fatal, but can in very severe cases cause coma and death.[13]
Solanidine is a very importantprecursor for thesynthesis ofhormones and somepharmacologically active compounds.[2] The idea to utilize Solanidine as a starting material came from a desire to utilize wasted potato glycoalkaloids from potato farming. It was found a successful starting material for the creation of steroid hormones, such as16-DPA, which is a common intermediate found in industry synthesis ofprogesterone andcortisone derivatives.[14] The final reaction consisted of nine steps to get from Solanidine to DPA with a 30% yield.
Solanidine was found to have a strong biomarker in relation to the varied cytochrome gene CYP2D6. Due to its natural variance CYP2D6 can affect the efficiency and safety of common medicines such as antidepressants and antipsychotics.[15] Solanidine was first found to be a biomarker in 2014 and was found in high concentrations in CYP2D6 poor metabolizers as well as in patients utilizing CYP2D6 inhibitors compared with rapid metabolizers. Using paroxetine, a CYP2D6 inhibitor, 95% of solanidine metabolism was stopped. Since consumption of potatoes is so common, solanidine can be used as a biomarker when studying CYP2D6 drug-drug interactions and improve CYP2D6 activity prediction.[15]
In 1994, Gunic and coworkers reported theelectrochemical oxidation of 3β-acetoxy-solanidine inCH3CN/CH2Cl2 1/1 withpyridine as a base. The corresponding iminium salts2 and3 were obtained in a 1/1 ratio in good yield. Performing thiselectrochemical reaction in DCM with pyridine gives3 in 95% yield, while the same reaction inacetone givesiminium salt2 in 95% yield.Iminium ion2 can be isomerized to the thermodynamically more stable enamine5. THis isomerization is believed to proceed via enamine4, which is thekinetic product.
In 1997, Gašiet al. reported a short procedure for the degradation of solanidine to16-Dehydropregnenolone acetate. Instead of applying the electrochemical oxidation,Hg(OAc)2 in acetone was used as oxidizing agent. The advantage of this reagent and solvent system was the ease of use and the selective formation ofiminium salt2, which spontaneously isomerized to enamine3 (94%). Thisenamine was then subjected to another isomerization, which yielded the more thermodynamically more stable enamine4.NaIO4-oxidation opened up the cyclic enamine and gave lactam5. Elimination of the lactam part withAl2O3 in benzene afforded in 34% 16-dehydropregnenolone acetate (DPA) (6). UsingK2CO3 in benzene followed by reacetylation produced6 in a lower yield (11%).
In 1968, Beisler and Sato synthesizedtomatidenol from solanidine, and reported the successful opening of the E ring of solanidine via thevon Braun reaction.[18][19] Only in case of acetylated solanidine the von Braun reaction gave the E ring-opened product in 78% yield.
Treatment of α-bromine withKOAc gave in good yield the β-diacetate, which could be reduced withred-Al in benzene.
These types of compounds can be ringclosed tospirosolane compounds as shown by Schreiber.
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