Neurotensin (8-13)
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Neurotensin (8-13)

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Neurotensin (8-13), the smallest active fragment of neurotensin, results in a decrease in cell-surface NT1 receptors (NTR1) density.

Peptide Inhibitors
Catalog number
CAS number
Molecular Formula
Molecular Weight
Neurotensin (8-13)
Size Price Stock Quantity
10 mg $199 In stock
500 mg $524 In stock
(2S)-2-[[(2S,3S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-[[(2S)-2-amino-5-(diaminomethylideneamino)pentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-3-methylpentanoyl]amino]-4-methylpentanoic acid
H-Arg-Arg-Pro-Tyr-Ile-Leu-OH; L-arginyl-L-arginyl-L-prolyl-L-tyrosyl-L-isoleucyl-L-leucine; NT(8-13); Neurotensin Fragment 8-13; N5-(Diaminomethylene)-L-ornithyl-N5-(diaminomethylene)-L-ornithyl-L-prolyl-L-tyrosyl-L-isoleucyl-L-leucine
White to Off-white Lyophilized Solid
>97% by HPLC
1.40±0.1 g/cm3 (Predicted)
Store at -20°C
Soluble in Water
InChI Key
Canonical SMILES
1.Neurotensin modulates the electrical activity of frog pituitary melanotropes via activation of a G-protein-coupled receptor pharmacologically related to both the NTS1 and nts2 receptors of mammals.
Belmeguenai A;Vaudry H;Leprince J;Vivet B;Cavelier F;Martinez J;Louiset E Neuroendocrinology. 2000 Dec;72(6):379-91.
The primary structure of frog neurotensin (fNT) has recently been determined and it has been shown that fNT is a potent stimulator of alpha-MSH secretion by frog pituitary melanotropes. In the present study, we have investigated the effects of fNT on the electrical activity of cultured frog melanotropes by using the patch-clamp technique and we have determined the pharmacological profile of the receptors mediating the effect of fNT. In the cell-attached configuration, fNT (10(-7) M) provoked an increase in the action current discharge followed by an arrest of spike firing. In the gramicidin-perforated patch configuration, fNT (10(-7) M) induced a depolarization accompanied by an increase in action potential frequency and a decrease in membrane resistance. Administration of graded concentrations (10(-10) to 10(-6) M) of fNT or the C-terminal hexapeptide NT(8-13) caused a dose-dependent increase in the frequency of action potentials with EC(50) of 2 x 10(-8) and 5 x 10(-9) M, respectively. The stimulatory effect of fNT was mimicked by various pseudopeptide analogs, with the following order of potency: Boc-[Trp(11)]NT(8-13) > Boc-[D-Trp(11)]NT(8-13) > Boc-[Lys(8,9), Nal(11)]NT(8-13) > Boc-[Psi11,12]NT(8-13).
2.The effects of systemic NT69L, a neurotensin agonist, on baseline and drug-disrupted prepulse inhibition.
Shilling PD;Richelson E;Feifel D Behav Brain Res. 2003 Jul 14;143(1):7-14.
Centrally administered neurotensin (NT) produces behavioral and biochemical effects that are very similar to the effects of antipsychotic drugs. Therefore, there is much interest in the potential use of NT agonists as antipsychotic drugs. We have previously reported that PD149163, a NT(8-13) analogue, produced effects on prepulse inhibition (PPI) of startle after systemic administration that were suggestive of an atypical antipsychotic-like drug profile. To determine if these effects are shared by other peripherally administered NT agonists, we tested the effects of NT69L, a recently developed NT agonist that penetrates the CNS, on drug-induced PPI deficits. In the first experiment, rats received subcutaneous (s.c.) injections of NT69L (vehicle, 0.08, 0.25, and 1.0mg/kg) followed 30min later by subcutaneous saline or D-amphetamine (2.0mg/kg). In the second experiment, NT69L injections were followed by saline or the non-competitive NMDA antagonist dizocilpine (0.1mg/kg). Both D-amphetamine and dizocilpine significantly decreased PPI as expected. In the first experiment, NT69L significantly increased PPI levels at baseline and after D-amphetamine. In the second experiment, NT69L attenuated PPI deficits produced by dizocilpine, without increasing baseline PPI.
3.Mesencephalic microinjections of neurotensin-(1-13) and its C-terminal fragment, neurotensin-(8-13), potentiate brain stimulation reward.
Rompré PP;Gratton A Brain Res. 1993 Jul 9;616(1-2):154-62.
Using the curve shift method, we assessed the effects of ventromedial mesencephalic tegmental (VMT) microinjections of an equimolar concentration of neurotensin-(1-13) (NT-(1-13)) and of its C-terminal fragment, neurotensin-(8-13) (NT-(8-13)), on operant responding for rewarding electrical stimulation of the caudal mesencephalic central gray. The effects of NT-(1-13) and NT-(8-13) on brain stimulation reward (BSR) were also compared to those of systemically administered quinpirole (0.1 and 0.2 mg/kg, s.c.), a direct dopamine agonist, and GBR-12909 (10 and 20 mg/kg, i.p.), a selective dopamine uptake blocker. At the concentration injected, NT-(8-13) was as effective as NT-(1-13) at facilitating BSR, producing significant leftward shifts of the function relating the rate of responding to the stimulation frequency (R/F function); neither form of the peptide was effective when injected in regions dorsal to the VMT. Similarly, GBR-12909 produced a parallel leftward shift of the R/F function, but, unlike NT-(1-13), also significantly increased the asymptotic rates of responding. In contrast, the high dose of quinpirole produced non-parallel leftward shifts of the R/F function and suppressed the asymptote.
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