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PPTN HCl

Alias: PPTN hydrochloride; 1992047-65-0; PPTN (hydrochloride); 4-(4-piperidin-4-ylphenyl)-7-[4-(trifluoromethyl)phenyl]naphthalene-2-carboxylic acid;hydrochloride; CHEMBL4743495;
Cat No.:V42083 Purity: ≥98%
PPTN HCl is a potent, high-affinity, competitive and selective P2Y14 receptor blocker (antagonist) with a KB of 434 pM.
PPTN HCl
PPTN HCl Chemical Structure CAS No.: 1992047-65-0
Product category: New2
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of PPTN HCl:

  • PPTN
  • PPTN Mesylate
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Top Publications Citing lnvivochem Products
Product Description
PPTN HCl is a potent, high-affinity, competitive and selective P2Y14 receptor blocker (antagonist) with a KB of 434 pM. PPTN HCl has no agonist or antagonist effects on P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, P2Y12 or P2Y13 receptors. Has anti~inflammatory and anti-immune activity.
Biological Activity I Assay Protocols (From Reference)
Targets
P2Y14 receptor (KB = 434 pM)
ln Vitro
In comparison to the other seven thiophene-activated P2Y traps, PPTN hydrochloride P2Y14-R exhibited more selectivity. When it comes to P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, P2Y12, and P2Y13 cannulas, 1 μM PPTN has neither analgesic nor antagonistic effects [1].
In secretory HL-60 human promyelocytes, PPTN inhibits UDP-concentration-promoted cell chemotaxis in leukocytes; in the presence of 10 μM UDP-concentration, IC50s are 1 nM; in the presence of 100 μM UDP-In the presence of glucose, IC50s are roughly 4 nM[1]. < br /> PPTN (10μM) dramatically lowers p-p38/p38 and p-ERK1/2/ERK1/2[2].
Researchers synthesized one of these molecules, a 4,7-disubstituted 2-naphthoic acid derivative (PPTN), and studied its pharmacological properties in detail. The concentration-effect curve of UDP-glucose for promoting inhibition of adenylyl cyclase in C6 glioma cells stably expressing the P2Y14-R was shifted to the right in a concentration-dependent manner by PPTN. Schild analyses revealed that PPTN-mediated inhibition followed competitive kinetics, with a KB of 434 pM observed. In contrast, 1 μM PPTN exhibited no agonist or antagonist effect at the P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, P2Y12, or P2Y13 receptors. UDP-glucose-promoted chemotaxis of differentiated HL-60 human promyelocytic leukemia cells was blocked by PPTN with a concentration dependence consistent with the KB determined with recombinant P2Y14-R. In contrast, the chemotactic response evoked by the chemoattractant peptide fMetLeuPhe was unaffected by PPTN. UDP-glucose-promoted chemotaxis of freshly isolated human neutrophils also was blocked by PPTN. In summary, this work establishes PPTN as a highly selective high-affinity antagonist of the P2Y14-R that is useful for interrogating the action of this receptor in physiologic systems. [1]
ln Vivo
Inhibition of the P2Y14 receptor in the trigeminal ganglion (TG) attenuated CFA-induced mechanical hyperalgesia [2]
A selective inhibitor of the P2Y14 receptor, 4-[4-(4-piperidinyl) phenyl]-7-[4-(trifluoromethyl) phenyl]-2-naphthalenecarboxylic acid hydrochloride (PPTN), was diluted in 0.05% dimethyl sulfoxide (DMSO). DMSO (0.05%) and PPTN were injected into the TG 30 min prior to CFA treatment. In Fig. 3A, compared to mechanical hyperalgesia in the CFA group, DMSO administration had no effect on mechanical hyperalgesia at 1 d (P > 0.05), 2 d (P > 0.05), and 3 d (P > 0.05) (n = 9 per group) (two-way RM ANOVA followed by Bonferroni test) [the main effect of treatment (F(3,24) = 315.696, P < 0.001), the main effect of time (F(3,24) = 22.192, P < 0.001), and the interaction effect (F(9,72) = 25.208, P < 0.001)]. However, compared to mechanical hyperalgesia in the CFA + DMSO group, the administration of 5 μM PPTN attenuated mechanical hyperalgesia at 1 d (P < 0.001), 2 d (P < 0.001), and 3 d (P < 0.05) (n = 9 per group), and the administration of 10 μM PPTN attenuated mechanical hyperalgesia at 1 d (P < 0.001), 2 d (P < 0.001), and 3 d (P < 0.001) (n = 9 per group). These results suggested that the inhibition of the P2Y14 receptor in the TG might modulate CFA-induced inflammatory pain.
Inhibition of the P2Y14 receptor in the TG decreased the CFA-induced upregulated expression of IL-1β, TNF-α, GFAP, and CCL2 [2]
Thirty minutes before CFA treatment, 0.05% DMSO and 10 μM PPTN were injected into the TG. The expression of the IL-1β, TNF-α, GFAP, and CCL2 proteins in the contralateral and ipsilateral TG was analyzed by western blot at 1 d after CFA injection. In Fig. 3C, D, E, and F, expression of the IL-1β, TNF-α, CCL2, and GFAP between the CFA group and the CFA + DMSO group were not significantly different (P > 0.05). As indicated in Fig. 3C, compared to the contralateral, IL-1β expression in ipsilateral was significantly increased by CFA treatment (P < 0.001). However, compared to CFA + DMSO group, 10 μM PPTN pretreatment reduced IL-1β expression (P < 0.01) (n = 3 per group). As indicated in Fig. 3D, the expression of TNF-α was significantly upregulated after CFA injection (P < 0.001, vs. contra). However, TNF-α was decreased by pretreatment with 10 μM PPTN (P < 0.05, vs. CFA + DMSO) (n = 3 per group). In Fig. 3E, GFAP expression was significantly increased by CFA treatment (P < 0.001, vs. contra) and then attenuated by 10 μM PPTN (P < 0.01, vs. CFA + DMSO) (n = 3 per group). The results in Fig. 3F indicated that CFA treatment significantly upregulated CCL2 expression (P < 0.001, vs. contra), which was decreased by 10 μM PPTN (P < 0.05, vs. CFA + DMSO) (n = 3 per group). The data above implied that P2Y14 receptor inhibition might attenuate mechanical hyperalgesia through inhibiting SGCs activation and decreasing IL-1β, TNF-α, and CCL2 expression in the TG.
Inhibition of the P2Y14 receptor decreased the CFA-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 [2]
The phosphorylation and activation of ERK1/2 and p38 are involved in inflammatory pain (Cady et al., 2014; Dong et al., 2014). After 0.05% DMSO and 10 μM PPTN were injected into the TG, the expression of p-ERK1/2 and p-p38 in the contralateral and ipsilateral TG was measured by western blot at 3 d after CFA treatment according to previous studies (Cady et al., 2014). In Fig. 4B and E, the integrated optical density (IOD) ratios of ERK1/2 to β-actin and p-38 to β-actin were not significantly different among the control group, the CFA group, the CFA + DMSO group, and the CFA + PPTN group (P > 0.05) (n = 3 per group). In Fig. 4C, CFA treatment enhanced the IOD ratio of p-ERK1/2 to ERK1/2 compared to that in the contralateral (P < 0.01) (n = 3 per group). The difference in the ratio of p-ERK1/2 to ERK1/2 between the CFA group and the CFA + DMSO group was not significant (P > 0.05). However, 10 μM PPTN significantly attenuated the ratio of p-ERK1/2 to ERK1/2 compared to that in the CFA + DMSO group (P < 0.01). In Fig. 4F, the IOD ratio of p-p38 to p38 was also increased after CFA injection (P < 0.01, vs. contra) (n = 3 per group). The ratio of p-p38 to p38 in the CFA group did not differ from that in the CFA + DMSO group (P > 0.05). However, the p-p38 to p38 ratio was significant lower following 10 μM PPTN pretreatment than in the CFA + DMSO group (P < 0.05) (n = 3 per group). These data suggested that the effects of the P2Y14 receptor on CFA-induced mechanical hyperalgesia might include the phosphorylation of ERK1/2 and p38 in the TG.
Cell Assay
Quantification of Cyclic AMP Accumulation. [1]
Cells were plated in 24-well plates approximately 24 hours before the assay and were labeled 2 hours before the assay with 1 µCi [3H]adenine/well in 25 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES)-buffered serum-free DMEM. All assays were in the presence of 200 µM 3-isobutyl-1-methylxanthine (IBMX) and were initiated by the addition of 30 μM forskolin, agonists, and/or PPTN. Incubations were for 15 minutes at 37°C and were terminated by aspiration of medium and addition of 500 µl ice-cold 5% trichloroacetic acid. [3H]Cyclic AMP was isolated by sequential Dowex and alumina chromatography (Salomon et al., 1974), as previously described (Harden et al., 1982).
Inositol Phosphate Accumulation in Cell Lines Stably Expressing P2Y Receptors. [1]
Stable 1321N1 human astrocytoma cell lines for each of the Gq/phospholipase C–coupled P2Y receptors (i.e., P2Y1-1321N1, P2Y2-1321N1, P2Y4-1321N1, P2Y6-1321N1, and P2Y11-1321N1 cells) were used in experiments designed to examine the P2Y-R subtype selectivity of PPTN. Cells were plated (20,000 cells/well) in 96-well plates two days before assay, and 16 hours before the assay, the inositol lipid pool of the cells was radiolabeled by incubation in 100 µl of serum-free inositol-free DMEM containing 1.0 µCi of myo-[3H]inositol. Incubations with drugs were in 20 mM HEPES (pH 7.4)–buffered Hanks' balanced salt solution (HBSS) containing 10 mM LiCl and were terminated after 30 minutes at 37°C by aspiration of the medium and addition of 50 mM formic acid. The samples were neutralized with 150 mM ammonium hydroxide, and [3H]inositol phosphate accumulation was quantified using Dowex chromatography and liquid scintillation counting, as previously described (Brown et al., 1991).
Quantification of Chemotaxis. [1]
Human neutrophils were loaded with 2.5 μM carbocyanide dye 1,1'-dioctadecyl-3,3,3′,3′-tetramethylindodicarbocyanine perchlorate (DID; Vybrant Cell-Labeling Solutions) for 15 minutes (106 cells/ml) in RPMI medium supplemented with 10% heat-inactivated FBS, and dHL-60 cells were loaded with 2.5 μM DID in HEPES-buffered (pH 7.4) HBSS supplemented with 1.6 mM CaCl2 and 0.8 mM MgCl2. Cells were rinsed twice and suspended in RPMI or HBSS as above. Chemotaxis was quantified in 96-multiwell FluoroBlock inserts as described previously (Sesma et al., 2012). In brief, vehicle or agonist was added to the lower compartment (225 μl), and 75-μl of a cell suspension (2 × 105 cells) was loaded onto the upper compartment in the absence or presence of the indicated amount of PPTN. The fluorescent signal (F, 612 nm excitation/670 nm emission) was read at the indicated times with use of a Tecan Infinite M1000 plate reader. The chemotaxis index (Ctx Index) was defined as: Ctx Index = (F1 – FB) ⁄ (F0 – FB), where F1 and F0 represent the fluorescence signal from stimulated and unstimulated cells, respectively, and FB is background fluorescence measured in the absence of cells. Typical values for fluorescence in these experiments were: F(B) = 180, F(0) = 1000, F(UDP-glucose) = 1300–1600; F[formyl-Met-Leu-Phe (fMLP)] = 2300–2500.
Animal Protocol
Trigeminal ganglion (TG) drug administration [2]
Trigeminal injection was performed according to a previous study (Long et al., 2017). Following anesthesia with isoflurane, facial hairs between the ears and eyes were removed with clippers. This area was disinfected with 10% Betadine. The injection site was between the notch and tympanic bulla; more specifically, the injection site was 2 mm posterior to the most anterior point on the notch. After the notch was palpated between the ipsilateral angular process and the condylar process, the rats were injected by Hamilton syringe in the medial–superior direction (90° to the head midline and 15° to the coronal plane). The needles were inserted to a depth of approximately 9 mm. Then, drugs were injected over 1 min, and the needles were held at the final position for 1 min before their slow removal. Thirty minutes before CFA injection, the rats were treated with dimethyl sulfoxide (DMSO diluted to 0.05%, 0.05 μl/g body weight; Sigma–Aldrich) and PPTN (5 μM or 10 μM dissolved in 0.05% DMSO, 0.05 μl/g body weight; Tocris Bioscience, UK). The concentration and volume of PPTN were chosen according to previous studies (Azroyan et al., 2015; Long et al., 2017; Sesma et al., 2016). Thus, rats were also randomly divided into four groups: the control group (contralateral whisker pad area injected with saline), the CFA group (ipsilateral whisker pad area injected with CFA, inflamed rats), the CFA + DMSO group (inflamed rats with ipsilateral trigeminal injection of 0.05% DMSO), and the CFA + PPTN group (inflamed rats with ipsilateral trigeminal injection of PPTN).
References

[1]. A selective high-affinity antagonist of the P2Y14 receptor inhibits UDP-glucose-stimulated chemotaxis of human neutrophils. Mol Pharmacol. 2013 Jul;84(1):41-9.

[2]. The P2Y14 receptor in the trigeminal ganglion contributes to the maintenance of inflammatory pain. Neurochem Int. 2019 Dec;131:104567.

Additional Infomation
The nucleotide-sugar-activated P2Y14 receptor (P2Y14-R) is highly expressed in hematopoietic cells. Although the physiologic functions of this receptor remain undefined, it has been strongly implicated recently in immune and inflammatory responses. Lack of availability of receptor-selective high-affinity antagonists has impeded progress in studies of this and most of the eight nucleotide-activated P2Y receptors. A series of molecules recently were identified by Gauthier et al. (Gauthier et al., 2011) that exhibited antagonist activity at the P2Y14-R.
UDP-glucose is released concomitantly with mucins (Hirschberg et al., 1998) from airway epithelial goblet (mucous) cells (Kreda et al., 2007; Okada et al., 2011), and chronic lung diseases, such as cystic fibrosis, asthma, and chronic obstructive lung disease, are characterized by mucin hypersecretion and inflammation. Potentially relevant to airway inflammation, UDP-glucose levels in lung secretions (i.e., bronchoalveolar lavage fluids) from patients with cystic fibrosis are in the range of concentrations that promote robust activation of the P2Y14-R (Sesma et al., 2009). Thus, the pharmacological activity and selectivity of PPTN for the P2Y14-R delineated here using recombinant cell systems indicates that this molecule should prove to be useful for interrogation of the physiologic roles of the P2Y14-R in lung inflammation in vivo. This notion is made more tangible by our observation that PPTN blocks UDP-glucose–promoted chemotaxis of human neutrophils and does so across a concentration range consistent with its KB determined in the P2Y14-R–expressing cell line.[1]
P2Y purinergic receptors expressed in neurons and satellite glial cells (SGCs) of the trigeminal ganglion (TG) contribute to inflammatory and neuropathic pain. P2Y14 receptor expression is reported in the spinal cord, dorsal root ganglion (DRG), and TG. In present study, the role of P2Y14 receptor in the TG in inflammatory orofacial pain of Sprague-Dawley (SD) rats was investigated. Peripheral injection of complete Freund's adjuvant (CFA) induced mechanical hyperalgesia with the rapid upregulation of P2Y14 receptor, glial fibrillary acidic protein (GFAP), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), C-C chemokine CCL2, phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), and phosphorylated p38 (p-p38) proteins in the TG. Furthermore, immunofluorescence staining confirmed the CFA-induced upregulation of P2Y14 receptor. Double immunostaining showed that P2Y14 receptor colocalized with glutamine synthetase (GS) and neuronal nuclei (NeuN). Finally, trigeminal injection of a selective antagonist (PPTN) of P2Y14 receptor attenuated CFA-induced mechanical hyperalgesia. PPTN also decreased the upregulation of the GFAP, IL-1β, TNF-α, CCL2, p-ERK1/2, and p-p38 proteins. Our findings showed that P2Y14 receptor in TG may contribute to orofacial inflammatory pain via regulating SGCs activation, releasing cytokines (IL-1β, TNF-α, and CCL2), and phosphorylating ERK1/2 and p38.[2]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C29H25CLF3NO2
Molecular Weight
511.962517499924
Exact Mass
511.152
Elemental Analysis
, 68.04; H, 4.92; Cl, 6.92; F, 11.13; N, 2.74; O, 6.25
CAS #
1992047-65-0
Related CAS #
PPTN;1160271-30-6; 1160271-31-7
PubChem CID
121513852
Appearance
White to off-white solid powder
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
6
Rotatable Bond Count
4
Heavy Atom Count
36
Complexity
705
Defined Atom Stereocenter Count
0
InChi Key
FKMVYPCBLWYNAV-UHFFFAOYSA-N
InChi Code
InChI=1S/C29H24F3NO2.ClH/c30-29(31,32)25-8-5-19(6-9-25)22-7-10-26-23(15-22)16-24(28(34)35)17-27(26)21-3-1-18(2-4-21)20-11-13-33-14-12-20;/h1-10,15-17,20,33H,11-14H2,(H,34,35);1H
Chemical Name
4-(4-piperidin-4-ylphenyl)-7-[4-(trifluoromethyl)phenyl]naphthalene-2-carboxylic acid;hydrochloride
Synonyms
PPTN hydrochloride; 1992047-65-0; PPTN (hydrochloride); 4-(4-piperidin-4-ylphenyl)-7-[4-(trifluoromethyl)phenyl]naphthalene-2-carboxylic acid;hydrochloride; CHEMBL4743495;
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO : ~250 mg/mL (~488.32 mM)
Solubility (In Vivo)
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

Injection Formulations
(e.g. IP/IV/IM/SC)
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution 50 μL Tween 80 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO 400 μLPEG300 50 μL Tween 80 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).
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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO 100 μLPEG300 200 μL castor oil 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (i.e. 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).
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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders


Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 1.9533 mL 9.7664 mL 19.5328 mL
5 mM 0.3907 mL 1.9533 mL 3.9066 mL
10 mM 0.1953 mL 0.9766 mL 1.9533 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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