Syrosingopine
Syrosingopine has selective depleting effect on brain amines is potentiated by combined treatment with disulfiram or fusaric acid, a dopamine beta-hydroxylase inhibitor. Syrosingopine can sensitize cancer cells to metformin and its more potent derivative phenformin far below the individual toxic threshold of each compound, thus, combining syrosingopine and codrugs is a promising therapeutic strategy for clinical application for the treatment of cancer.Syrosingopine also has hypotensive properties.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Sci. Adv.,2016 Dec; 2(12): e1601756.
Syrosingopine sensitizes cancer cells to killing by metformin[Pubmed:
28028542]
METHODS AND RESULTS:
We report that the anticancer activity of the widely used diabetic drug metformin is strongly potentiated by Syrosingopine. Synthetic lethality elicited by combining the two drugs is synergistic and specific to transformed cells. This effect is unrelated to Syrosingopine’s known role as an inhibitor of the vesicular monoamine transporters. Syrosingopine binds to the glycolytic enzyme α-enolase in vitro, and the expression of the γ-enolase isoform correlates with nonresponsiveness to the drug combination. Syrosingopine sensitized cancer cells to metformin and its more potent derivative phenformin far below the individual toxic threshold of each compound.
CONCLUSIONS:
Thus, combining Syrosingopine and codrugs is a promising therapeutic strategy for clinical application for the treatment of cancer.
C R Seances Soc Biol Fil. 1960;154:55-7.
Hypertensive action of syrosingopine after ephedrine.[Pubmed:
14443141]
METHODS AND RESULTS:
Hypertensive action of Syrosingopine after ephedrine.
Pharmacol Biochem Behav. 1986 May;24(5):1457-9.
Effects of amnesic doses of reserpine or syrosingopine on mouse brain acetylcholine levels.[Pubmed:
2873591]
The effects of reserpine and Syrosingopine on mouse whole brain acetylcholine levels were examined.
METHODS AND RESULTS:
At 2 or 24 hr following injection, the brains were removed and analyzed by mass spectrometry. No differences were found between drug-treated and control mice in the acetylcholine content of the brain at either time interval.
CONCLUSIONS:
The results suggest that whole brain acetylcholine levels do not predict the amnesic effects of either reserpine or Syrosingopine.
Behav Neural Biol. 1983 May;38(1):120-6.
The effect of reserpine, syrosingopine, and guanethidine on the retention of discriminated escape reversal: peripherally administered catecholamines cannot reverse the reserpine amnesia in this situation.[Pubmed:
6138025]
METHODS AND RESULTS:
In a series of experiments, the effects of reserpine, Syrosingopine, and guanethidine on retention of a discriminated escape reversal training were investigated in mice. The peripherally and centrally acting reserpine produced amnesia while the primarily peripherally acting compounds, Syrosingopine or guanethidine, did not produce amnesia even when given in high dosages or when training was given with low footshock.
CONCLUSIONS:
Unlike in the passive avoidance situation, peripherally administered norepinephrine or dopamine was not able to attenuate the reserpine-induced amnesia. The results were discussed in terms of the role of biogenic amines in memory formation.
Pharmacol Biochem Behav. 1976 Apr;4(4):419-25.
Selective depleting effect of syrosingopine on brain catecholamine levels with relation to morphine analgesia in the rat.[Pubmed:
6976 ]
Reserpine was the most potent, rescinnamine the next and Syrosingopine the weakest in the depleting effects on brain amines of rauwolfia alkaloids.
METHODS AND RESULTS:
After Syrosingopine, brain dopamine (DA) was decreased to a smaller degree and with a shorter duration as compared with norepinephrine (NE) and serotonin (5-HT), whereas reserpine elicited a marked and long lasting reduction in these amines. Accordingly, Syrosingopine induced a depletion of brain NE and 5-HT without alteration in brain DA content 2-4 days after administration. Repeated administrations of Syrosingopine, 2 mg/kg daily for 2 or 4 days, resulted in similar alterations in brain amine levels. This selective depleting effect of Syrosingopine on brain amines was potentiated by combined treatment with disulfiram or fusaric acid, a dopamine beta-hydroxylase inhibitor. Under the condition of selective depletion of brain amines induced by repeated administrations of Syrosingopine, 2 mg/kg daily for 2 days, the analgesic action of morphine was not affected, whereas reserpine and tetrabenazine antagonized morphine analgesia, concomitant with inducing a depletion of all brain amines.
CONCLUSIONS:
The results suggest that brain DA may be more important than brain NE or 5-HT with regard to the mechanisms by which morpine produces analgesia.
