LY 311727

Selective secreted phospholipase A2 (sPLA2) inhibitor CAS# 164083-84-5

LY 311727

Catalog No. BCC7728----Order now to get a substantial discount!

Product Name & Size Price Stock
LY 311727:10mg $215.00 In stock
LY 311727:20mg $366.00 In stock
LY 311727:50mg $860.00 In stock
LY 311727:100mg $1505.00 In stock
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Chemical structure

LY 311727

3D structure

Chemical Properties of LY 311727

Cas No. 164083-84-5 SDF Download SDF
PubChem ID 155922 Appearance Powder
Formula C22H27N2O5P M.Wt 430.43
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO and to 100 mM in 1eq. NaOH
Chemical Name 3-[3-(2-amino-2-oxoethyl)-1-benzyl-2-ethylindol-5-yl]oxypropylphosphonic acid
SMILES CCC1=C(C2=C(N1CC3=CC=CC=C3)C=CC(=C2)OCCCP(=O)(O)O)CC(=O)N
Standard InChIKey OPWQYOUZRHDKBR-UHFFFAOYSA-N
Standard InChI InChI=1S/C22H27N2O5P/c1-2-20-19(14-22(23)25)18-13-17(29-11-6-12-30(26,27)28)9-10-21(18)24(20)15-16-7-4-3-5-8-16/h3-5,7-10,13H,2,6,11-12,14-15H2,1H3,(H2,23,25)(H2,26,27,28)
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.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of LY 311727

DescriptionSelective secreted phospholipase A2 (sPLA2) inhibitor (IC50 values are <1 μM for group IIA and <50 μM for group V). Attenuates VEGF-mediated platelet-activating factor (PAF) synthesis in BAEC and HUVEC cells at a concentration of 100 μM.

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Preparing Stock Solutions of LY 311727

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3233 mL 11.6163 mL 23.2326 mL 46.4652 mL 58.0815 mL
5 mM 0.4647 mL 2.3233 mL 4.6465 mL 9.293 mL 11.6163 mL
10 mM 0.2323 mL 1.1616 mL 2.3233 mL 4.6465 mL 5.8081 mL
50 mM 0.0465 mL 0.2323 mL 0.4647 mL 0.9293 mL 1.1616 mL
100 mM 0.0232 mL 0.1162 mL 0.2323 mL 0.4647 mL 0.5808 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on LY 311727

Clinical and immunohistochemical performance of lyophilized platelet-rich fibrin (Ly-PRF) on tissue regeneration.[Pubmed:28192870]

Clin Implant Dent Relat Res. 2017 Jun;19(3):466-477.

BACKGROUND: Platelet-rich fibrin (PRF) has been widely used in oral implantology and other fields, but benefits of the fresh PRF (FPRF (fresh platelet-rich fibrin)) were consequently limited because of its short-term application. Thus, a protocol for the combination of PRF and lyophilization comes up in the present study to address the issue of PRF storage and delayed clinical application, which has little been reported in this field at home and abroad by now. PURPOSE: The aim of the present study was to evaluate the applicability of lyophilized platelet-rich fibrin (Ly-PRF) used as the scaffold material for craniofacial tissue regeneration and to compare its biochemical properties with commonly used fresh PRF. MATERIALS AND METHODS: Two volunteers with both genders were selected as the source of PRF and Ly-PRF samples. Macro- and micro-scopic appearance evaluation as well as immunohistochemical comparison were performed on PRF samples before and after freeze-drying at -196 degrees C. The second experimental phase was to observe clinical performance when fresh and lyophilized PRF were applied in guided bone regeneration (GBR) operations in 39 patients losing teeth in the anterior maxillary region who required an oral implantation followed by labial bone grafting. RESULTS: The conventional histological and transmission electron microscopy images showed the microstructure of Ly-PRF, which resembled a mesh containing apparently irregularly shaped platelets with less alpha-granule than fresh PRF in micro and a translucent membrane with less elasticity than fresh PRF in macro. Simultaneous immunohistological staining results showed positive expression of PDGF-BB, IL-1, IL-4, TNF, TGF-beta1 in both fresh and lyophilized PRF, while the expression of PDGF-BB, IL-1, TNF, TGF-beta1 has no statistical difference between them (P > .05) but that of IL-4 in Ly-PRF is statistically higher than in fresh PRF (P < .05). When applied in GBR operations, there were no significant differences between Ly-PRF and FPRF in factors of histological and clinical evaluations (i.e., color, swelling, bleeding of the mucosa, pain leveland, and remodeling of hard tissue) performed 3 days, 7 days, and 4 months after the surgery (P > .05). CONCLUSIONS: This study strongly supports that lyophilization at -196 degrees C does not largely influence the expression of bioactive factors, the microstructure of fibrinogen or the clinical effects of PRF.

Expansion of CD11b(+)Ly-6C(+) myeloid-derived suppressor cells (MDSCs) driven by galectin-9 attenuates CVB3-induced myocarditis.[Pubmed:28110209]

Mol Immunol. 2017 Mar;83:62-71.

Galectin-9 is known to play a role in the modulation of innate and adaptive immunity to ameliorate CVB3-induced myocarditis. In the present study, we found that galectin-9 induced the expansion of CD11b(+)Ly-6C(+) myeloid-derived suppressor cells (MDSCs) in the heart from CVB3-infected mice. Adoptive transfer of CD11b(+)Ly-6C(+) MDSCs significantly alleviated myocarditis accompanied by increased Th2 and Treg frequency and anti-inflammatory cytokines expression in the heart tissue. Moreover, Ly6C(+) MDSCs, but not Ly6G(+) cells, expressed Arg-1 and NOS2, and suppressed CD4(+) T cell proliferation in vitro in an Arg-1-dependent mechanism; an event that was reversed with treatment of either an Arg-1 inhibitor or addition of excess l-arginine. Furthermore, Ly6C(+) MDSCs co-expressed higher levels of F4/80, Tim-3, and IL-4Ralpha, and had the plasticity to up-regulate NOS2 or Arg-1 in response to IFN-gamma or IL-4 treatment. The present results indicate that galectin-9 expands CD11b(+)Ly-6C(+) MDSCs to ameliorate CVB3-induced myocarditis.

Assessment of roles for the Rho-specific guanine nucleotide dissociation inhibitor Ly-GDI in platelet function: a spatial systems approach.[Pubmed:28148498]

Am J Physiol Cell Physiol. 2017 Apr 1;312(4):C527-C536.

On activation at sites of vascular injury, platelets undergo morphological alterations essential to hemostasis via cytoskeletal reorganizations driven by the Rho GTPases Rac1, Cdc42, and RhoA. Here we investigate roles for Rho-specific guanine nucleotide dissociation inhibitor proteins (RhoGDIs) in platelet function. We find that platelets express two RhoGDI family members, RhoGDI and Ly-GDI. Whereas RhoGDI localizes throughout platelets in a granule-like manner, Ly-GDI shows an asymmetric, polarized localization that largely overlaps with Rac1 and Cdc42 as well as microtubules and protein kinase C (PKC) in platelets adherent to fibrinogen. Antibody interference and platelet spreading experiments suggest a specific role for Ly-GDI in platelet function. Intracellular signaling studies based on interactome and pathways analyses also support a regulatory role for Ly-GDI, which is phosphorylated at PKC substrate motifs in a PKC-dependent manner in response to the platelet collagen receptor glycoprotein (GP) VI-specific agonist collagen-related peptide. Additionally, PKC inhibition diffuses the polarized organization of Ly-GDI in spread platelets relative to its colocalization with Rac1 and Cdc42. Together, our results suggest a role for Ly-GDI in the localized regulation of Rho GTPases in platelets and hypothesize a link between the PKC and Rho GTPase signaling systems in platelet function.

Short-term dabigatran interruption before cardiac rhythm device implantation: multi-centre experience from the RE-LY trial.[Pubmed:28339794]

Europace. 2017 Oct 1;19(10):1630-1636.

Aims: Cardiac implantable electronic device (CIED) surgery is commonly performed in patients with atrial fibrillation (AF). The current analysis was undertaken to compare peri-operative anticoagulation management, bleeding, and thrombotic events in AF patients treated with dabigatran vs. warfarin. Methods and results: This study included 611 patients treated with dabigatran vs. warfarin who underwent CIED surgery during the RE-LY trial. Among 201 warfarin-treated patients, warfarin was interrupted a median of 144 (inter-quartile range, IQR: 120-216) h, and 37 (18.4%) patients underwent heparin bridging. In dabigatran-treated patients (216 on 110 mg bid and 194 on 150 mg bid), the duration of dabigatran interruption was a median of 96 (IQR: 61-158) h. Pocket hematomas occurred in 9 (2.20%) patients on dabigatran and 8 (3.98%) patients on warfarin (P = 0.218). The occurrence of pocket hematomas was lower with dabigatran compared with warfarin with heparin bridging (RD: -8.62%, 95% CI: -24.15 to - 0.51%, P = 0.034) but not when compared with warfarin with no bridging (P = 0.880). Ischemic stroke occurred in 2 (0.3%) patients; one in the warfarin group (without bridging) and one in the dabigatran 150 mg bid group (P = 0.735). Conclusion: In patients treated with dabigatran undergoing CIED surgery, interruption of dabigatran is associated with similar or lower incidence of pocket hematoma, when compared with warfarin interruption without or with heparin bridging, respectively. Whether uninterrupted dabigatran can reduce pocket hematoma or ischemic stroke remains to be evaluated.

VEGF stimulation of endothelial cell PAF synthesis is mediated by group V 14 kDa secretory phospholipase A2.[Pubmed:11522612]

Br J Pharmacol. 2001 Sep;134(1):197-205.

1. Vascular endothelial growth factor (VEGF) is a potent inducer of inflammation, and we have shown that this latter effect is mediated through endothelial cell (EC) PAF synthesis. Since the phospholipid remodelling pathway enzymes (CoA-independent transacylase, CoA-IT; phospholipase A2, PLA2; and lyso-PAF acetyltransferase, lyso-PAF-AT) may participate in PAF synthesis, we assessed their contribution to VEGF-induced PAF synthesis in bovine aortic EC (BAEC) and human umbilical vein EC (HUVEC). 2. VEGF enhanced BAEC and HUVEC PAF synthesis by up to 28 and 4 fold above basal levels respectively. 3. A pretreatment with a CoA-IT and lyso-PAF-AT inhibitor (Sanguinarin; 500 nM) blocked VEGF-induced PAF synthesis by 95%, a specific CoA-IT inhibitor (SKF45905; 10 - 50 microM) was without effect, confirming the crucial role of the PLA2 and lyso-PAF-AT. 4. Treatment with secreted PLA2 (sPLA2) inhibitors which have been shown to inhibit both groups IIA and V sPLA2 (SB203347; 10 microM and LY311727; 100 microM) blocked EC PAF synthesis by up to 90%, whereas selective inhibition of group IIA sPLA2 (LY311727; 1 microM) had no significant effect. 5. RT - PCR and Western blot analyses demonstrated the presence of group V sPLA2 whereas group IIA sPLA2 was undetected in EC. 6. Treatment with cytosolic and calcium-independent PLA2 inhibitors (Arachidonyl trifluoromethyl ketone, Bromoenol lactone, Methyl arachydonyl fluorophosphate, up to 50 microM) did not prevent but rather potentiated the VEGF effect on EC PAF synthesis. 7. These results provide evidence that with VEGF activation of EC cells, the group V sPLA2 provides substrate for EC PAF formation.

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