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[Sar9,Met(O2)11]-Substance P

[Sar9,Met(O2)11]-Substance P

Catalog No. BCC6960
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1mg $160.00 Ship Within 7 Days
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Quality Control of [Sar9,Met(O2)11]-Substance P

Chemical structure

[Sar9,Met(O2)11]-Substance P

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Chemical Properties of [Sar9,Met(O2)11]-Substance P

Cas No. 110880-55-2 SDF Download SDF

(Modifications: X = Sar, Met-11 = Met(O2), Met-11 = C-terminal amide)

Standard InChI InChI=1S/C64H100N18O15S/c1-38(2)34-46(57(89)74-42(54(69)86)28-33-98(4,96)97)73-53(85)37-80(3)62(94)48(36-40-18-9-6-10-19-40)79-58(90)47(35-39-16-7-5-8-17-39)78-56(88)43(24-26-51(67)83)75-55(87)44(25-27-52(68)84)76-59(91)50-23-15-32-82(50)63(95)45(21-11-12-29-65)77-60(92)49-22-14-31-81(49)61(93)41(66)20-13-30-72-64(70)71/h5-10,16-19,38,41-50H,11-15,20-37,65-66H2,1-4H3,(H2,67,83)(H2,68,84)(H2,69,86)(H,73,85)(H,74,89)(H,75,87)(H,76,91)(H,77,92)(H,78,88)(H,79,90)(H4,70,71,72)/t41-,42-,43-,44-,45-,46-,47-,48-,49-,50-/m0/s1
Formula C64H100N18O15S M.Wt 1393
Solubility Soluble to 1 mg/ml in water
Storage Desiccate at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

References on [Sar9,Met(O2)11]-Substance P

Anti-nociceptive effects of selectively destroying substance P receptor-expressing dorsal horn neurons using [Sar9,Met(O2)11]-substance P-saporin: behavioral and anatomical analyses.[Pubmed: 17418497]

Lumbar intrathecal injections of substance P-saporin (SP-sap) destroy dorsal horn neurons that express the neurokinin-1 receptor (NK-1R) resulting in decreased responses to a range of noxious stimuli and decreased hyperalgesia and allodynia. Forebrain injections of SP-sap produce considerable non-specific damage raising some concern about use of this toxin in vivo. The more stable and selective substance P congener, [Sar9,Met(O2)11]substance P coupled to saporin (SSP-sap) produces much more selective forebrain lesions at significantly lower doses. The present study sought to determine the anatomic and nocifensive behavioral effects of lumbar intrathecal injections of the more precisely targeted SSP-sap. On the basis of loss of lamina I NK-1R staining, lumbar intrathecal SSP-sap was seven times more potent than SP-sap and produced no loss of NK-1R expressing neurons in deeper laminae (III-VI or X). Transient decreases in hotplate responding occurred at 44 degrees C and 47 degrees C but not 52 degrees C during the first 3 weeks after SSP-sap injection with return to baseline by 4 weeks. Operant escape responses were reduced at 0.3 degrees C, 44 degrees C and 47 degrees C for at least 4 months. In the formalin test, SSP-sap also was about seven times more potent than SP-sap in reducing phase two behavior in both female Long Evans and male Sprague-Dawley rats. Both SSP-sap and SP-sap reduced formalin-induced FOS expression in deep and superficial laminae of the L4 dorsal horn in parallel with the reduction in phase 2 behavior. In summary, SSP-sap is highly effective in destroying lamina I NK-1R expressing neurons, without loss of deep NK-1R neurons. The behavioral effects of SSP-sap are similar to SP-sap suggesting that the antinociceptive effects of both toxins are indeed due to selective loss of NK-1R neurons in lamina I. SSP-sap is an attractive agent for possible treatment of chronic pain.

Ava[L-Pro9,N-MeLeu10] substance P(7-11) (GR 73632) and Sar9, Met(O2)11 increase distention-induced peristalsis through activation of neurokinin-1 receptors on smooth muscle and interstitial cells of cajal.[Pubmed: 16330493]

Substance P is generally considered an excitatory neurotransmitter related to gut motor activity, although an inhibitory influence of neurokinin-1 (NK1) receptor activation on peristalsis has also been reported. With an optimized in vitro method to assess distention-induced peristalsis, our aim was to clarify the effect of NK1 receptor activation on peristaltic activity and to reveal the mechanisms by which NK1 activation alters peristalsis. Distention of the small intestine of the mouse and guinea pig induced periodic occurrence of rhythmic waves of propagating rings of circular muscle contraction, associated with slow waves and superimposed action potentials, that propelled intestinal contents aborally. Activation of NK1 receptors by Ava[l-Pro(9),N-MeLeu10] substance P(7-11) (GR 73632) and Sar(9), Met(O(2))(11) on smooth muscle cells resulted in prolongation of the activity periods and increased action potential generation occurring superimposed on the intestinal slow wave activity. Activation of NK1 receptors on interstitial cells of Cajal resulted in an increase in slow wave frequency. Slow wave amplitude increased, likely by increased cell-to-cell coupling. The NK1 antagonist (S)-1-(2-[3-(3,4-dichlorophenyl)-1-(3-isopropoxyphenylacetyl)piperidin-3-yl]ethyl)-4-phenyl-1-azoniabicyclo[2.2.2]octane chloride (SR 140333) induced a decrease in the slow wave frequency and duration of the activity periods evoked by distention, which makes it likely that NK1 receptor activation plays a role in the normal physiological distention-induced generation of peristaltic motor patterns. In summary, NK1 receptors play a role in normal development of peristalsis and NK1 receptor activation markedly increases propulsive peristaltic contractile activity.

[Intrathecal injection of Sar9, Met(O2)11-substance P, neurokinin-1 receptor agonist, increases nitric oxide synthase expression and nitric oxide production in the rat spinal cord].[Pubmed: 14695485]

In the spinal cord, nitric oxide (NO) pathway is involved in pain and hyperalgesia, and nitric oxide synthase (NOS) expression and NO production are upregulated following several noxious and lesion stimuli. However, the mechanism of the increases is yet not well understood. The present study was designed to address the question of whether substance P (SP) released in the spinal cord enhances NOS expression and NO production of the spinal cord in rats. [Sar(9), Met(O2)(11)]-substance P (Sar-SP), a neurokinin-1 (NK-1) receptor agonist, was administered by intrathecal injection via L(5)-L(6) intervertebral space to induce nociception. The pain threshold was determined by hot water induced tail flick test. NOS expression of the L(5) segment of the spinal cord was determined using NADPH-d histochemical staining. NO production of the lumbar enlargement of the spinal cord was determined by assaying NO3(-) and NO2(-), the end product of NO metabolism, using the method of aqua fortis reduction. We found that (1) intrathecal injection of Sar-SP (6.5 nmol) elicited a characteristic, caudally directed, nociceptive behavioural response consisting of intense biting, licking and scratching episodes. Tail flick test showed decrease in pain threshold. (2) following the behavioural responses, the NOS expression level, including the number and the staining density of the NADPH-d reactive cells, increased in the superficial portion of the dorsal horn (Laminae I-II) and the grey matter surrounding the central canal (LaminaX) of the L(5) segment of the spinal cord after the Sar-SP intrathecal injection. At the same time, NO production in the enlargement of the spinal cord increased. (3) The decreased pain threshold and the increases in NOS expression and NO production could be substantially inhibited by intrathecal injection of [[D-Arg(1), D-Trp(7,9), Leu(11)]-substance P] (spantide) (5 microg), a non-selective antagonist of NK-1 receptor, 5 min prior to the Sar-SP injection. It might be concluded that the release of SP resulted from nociceptive afferents increased NOS expression and NO production of the rat spinal cord.

Targeting neurokinin-1 receptor-expressing neurons with [Sar9,Met(O2)11 substance P-saporin.[Pubmed: 10643883]

Neurons expressing neurokinin-1 receptors (NK-1R) are selectively destroyed by substance P (SP) coupled to the ribosome inactivating protein, saporin. SP-saporin produces incomplete lesions of striatal NK-1R-expressing neurons even at doses that produce non-specific damage. In the present study, we sought to determine if the more stable, NK-1R-specific SP analog conjugated to saporin, [Sar9,Met(O2)11]-SP (SSP-saporin), would selectively destroy cells expressing NK-1R, in vitro and in vivo. The results show that SSP-saporin is highly effective and selective, producing extensive ablation of striatal NK-1R expressing interneurons at doses that do not cause loss of other striatal neurons suggesting advantages over SP-saporin as a selective lesioning agent. SSP-saporin will be useful in larger species and for intraparenchymal injections.


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