L-Aspartyl-L-Proline
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Others |
| Catalog number | BBF-05386 |
| CAS | 42155-95-3 |
| Molecular Weight | 230.22 |
| Molecular Formula | C9H14N2O5 |
| Purity | ≥98% |
Online Inquiry
Description
L-Aspartyl-L-Proline is a dipeptide composed of aspartic acid and proline. It is an incomplete breakdown product of protein digestion or protein catabolism.
Specification
| Synonyms | Aspartyl-L-proline; Aspartyl-proline; L-α-Aspartyl-L-proline; Aspartylproline; Asp-pro; 1-L-alpha-aspartyl-L-Proline; (S)-1-((S)-2-Amino-3-carboxypropanoyl)pyrrolidine-2-carboxylic acid; L-alpha-Aspartyl-L-proline |
| Sequence | H-Asp-Pro-OH |
| IUPAC Name | (2S)-1-[(2S)-2-amino-3-carboxypropanoyl]pyrrolidine-2-carboxylic acid |
| Canonical SMILES | C1CC(N(C1)C(=O)C(CC(=O)O)N)C(=O)O |
| InChI | InChI=1S/C9H14N2O5/c10-5(4-7(12)13)8(14)11-3-1-2-6(11)9(15)16/h5-6H,1-4,10H2,(H,12,13)(H,15,16)/t5-,6-/m0/s1 |
| InChI Key | UKGGPJNBONZZCM-WDSKDSINSA-N |
Properties
| Appearance | Solid |
| Boiling Point | 534.9±50.0°C at 760 mmHg |
| Density | 1.485 g/cm3 |
| Solubility | Soluble in Water |
Reference Reading
1. Combination treatment with N-acetyl-seryl-aspartyl-lysyl-proline and tissue plasminogen activator provides potent neuroprotection in rats after stroke
Li Zhang, Michael Chopp, Hua Teng, Guangliang Ding, Quan Jiang, Xiao Ping Yang, Nour Eddine Rhaleb, Zheng Gang Zhang Stroke. 2014 Apr;45(4):1108-14. doi: 10.1161/STROKEAHA.113.004399. Epub 2014 Feb 18.
Background and purpose: N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP), an endogenously produced circulating peptide in humans and rodents, exerts anti-inflammatory and cardioprotective activities in various cardiovascular diseases. Methods: The present study evaluated the neuroprotective effect of AcSDKP alone and in combination with thrombolytic therapy in a rat model of embolic focal cerebral ischemia. Results: We found that treatment with AcSDKP alone at 1 hour or the combination treatment with AcSDKP and tissue plasminogen activator (tPA) at 4 hours after stroke onset substantially increased AcSDKP levels in plasma and cerebrospinal fluid and robustly reduced infarct volume and neurological deficits, without increasing the incidence of brain hemorrhage compared with ischemic rats treated with saline, AcSDKP alone at 4 hours, and tPA alone at 4 hours. Moreover, the combination treatment considerably reduced the density of nuclear transcription factor-κB (NF-κB), transforming growth factor β (TGF-β), and plasminogen activator inhibitor-1 (PAI-1) positive cerebral blood vessels in the ischemic brain, all of which were associated with reduced microvascular fibrin extravasation and platelet accumulation compared with tPA monotherapy. In vitro, AcSDKP blocked fibrin-elevated TGF-β1, PAI-1, and NF-κB proteins in primary human brain microvascular endothelial cells. Conclusions: Our data indicate that AcSDKP passes the blood-brain barrier, and that treatment of acute stroke with AcSDKP either alone at 1 hour or in combination with tPA at 4 hours of the onset of stroke is effective to reduce ischemic cell damage in a rat model of embolic stroke. Inactivation of TGF-β and NF-κB signaling by AcSDKP in the neurovascular unit may underlie the neuroprotective effect of AcSDKP.
2. Potent and fully noncompetitive peptidomimetic inhibitor of multidrug resistance P-glycoprotein
Ophélie Arnaud, Ali Koubeissi, Laurent Ettouati, Raphaël Terreux, Ghina Alamé, Catherine Grenot, Charles Dumontet, Attilio Di Pietro, Joëlle Paris, Pierre Falson J Med Chem. 2010 Sep 23;53(18):6720-9. doi: 10.1021/jm100839w.
N(α)-Boc-l-Asp(OBn)-l-Lys(Z)-OtBu (reversin 121, 1), an inhibitor of the P-gp ABC transporter, was used to conceive compounds inhibiting the drug efflux occurring through the Hoechst 33342 and daunorubicin transport sites of P-gp, respectively H and R sites. Replacement of the aspartyl residue by trans-4-hydroxy-l-proline (4(R)Hyp) gave compounds 11 and 15 characterized by half-maximal inhibitory concentrations (IC(50)) of 0.6 and 0.2 μM, which are 2- and 7-fold lower than that of the parent molecule. The difference in IC(50) between 11 and 15 rests on the carbonyl group of the peptidyl bond, reduced in 15. Those compounds are rather specific of P-gp, having no or limited activity on MRP1 and BCRP. 15 displayed no marked cytotoxicity up to 10-fold its IC(50). Importantly, 15 equally inhibited the Hoechst 33342 and daunorubicin effluxes through a typical noncompetitive inhibition mechanism, suggesting its binding to a site different from the H and R drug-transport sites.
3. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline Augments Thrombolysis of tPA (Tissue-Type Plasminogen Activator) in Aged Rats After Stroke
Chao Li, Li Zhang, Chunyang Wang, Hua Teng, Baoyan Fan, Michael Chopp, Zheng Gang Zhang Stroke. 2019 Sep;50(9):2547-2554. doi: 10.1161/STROKEAHA.119.026212. Epub 2019 Aug 7.
Background and Purpose- Stroke is a leading cause of disability worldwide, mainly affecting the elderly. However, preclinical studies in aged ischemic animals are limited. N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is a naturally occurring tetrapeptide with vascular-protective properties. The present study investigated the effect of AcSDKP on tPA (tissue-type plasminogen activator)-induced thrombolysis in aged rats after ischemic stroke. Methods- Aged male rats (18 months) were subjected to embolic middle cerebral artery occlusion. Rats subjected to 4 hours of middle cerebral artery occlusion were randomized into the following groups: (1) AcSDKP; (2) tPA; (3) AcSDKP in combination with tPA; and (4) saline. Neurological deficits, cerebral microvascular patency and integrity, and infarction were examined at 1 day and 7 days after middle cerebral artery occlusion. In vitro experiments were performed to examine the effect of AcSDKP on aged cerebral endothelial cell permeability. Results- Compared with saline, AcSDKP, or tPA as monotherapy did not have any therapeutic effects, whereas AcSDKP in combination with tPA significantly reduced cerebral tissue infarction and improved neurological outcome without increasing cerebral hemorrhage. Concurrently, the combination treatment significantly augmented microvascular perfusion and reduced thrombosis and blood-brain barrier leakage. In vitro, compared with cerebral endothelial cells from ischemic adult rats, the endothelial cells from ischemic aged rats exhibited significantly increased leakage. AcSDKP suppressed tPA-induced aged endothelial cell leakage and reduced expression of ICAM-1 (intercellular adhesion molecule 1) and NF (nuclear factor)-κB. Conclusions- The present study provides evidence for the therapeutic efficacy of AcSDKP in combination tPA for the treatment of embolic stroke in aged rats at 4 hours after stroke onset. AcSDKP likely acts on cerebral endothelial cells to enhance the benefits of tPA by increasing tissue perfusion and augmenting the integrity of the blood-brain barrier. Visual Overview- An online visual overview is available for this article.
Recommended Products
| BBF-01826 | Deoxymannojirimycin | Inquiry |
| BBF-00764 | Cerebroside C | Inquiry |
| BBF-02614 | Nystatin | Inquiry |
| BBF-01825 | Loganin | Inquiry |
| BBF-03754 | CASTANOSPERMINE | Inquiry |
| BBF-03755 | Actinomycin D | 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 ╳
