5-HT_4A Receptor ( pKi = 8.6 ); 5-HT_4B Receptor ( pKi = 8.1 )
Prucalopride (R-108512, R-93877) is a selective and high-affinity agonist of the 5-hydroxytryptamine 4 (5-HT₄) receptor. It exhibits nanomolar affinity for human 5-HT₄(a) and 5-HT₄(b) receptor subtypes, with a Ki value of 0.9 nM for 5-HT₄(a) and 1.8 nM for 5-HT₄(b) in radioligand binding assays [1]
- In studies on gastrointestinal (GI) tissues, Prucalopride showed specific activation of 5-HT₄ receptors in colonic smooth muscle cells, with no significant binding to other 5-HT receptor subtypes (e.g., 5-HT₁, 5-HT₂, 5-HT₃) or non-serotonergic receptors (e.g., dopamine D₂, muscarinic M₃), as confirmed by displacement assays [3]

In vitro activity: Prucalopride has a pEC50 of 7.5 and causes contractions in a concentration-dependent manner. When electrical field stimulation is applied to the proximal colon of guinea pigs, the rebound contraction is greatly enhanced by pruralopride (1 mM). A monophasic concentration–response curve is produced when prucalopride relaxes the rat oesophagus preparation of rat oesophagus tunica muscularis mucosae, with a pEC50 of 7.8. [1]

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In isolated guinea pig colon segments, Prucalopride concentration-dependently increased smooth muscle contraction amplitude. The EC₅₀ for this contractile effect was 3.2 nM, and the maximum contraction amplitude reached 145% of the response induced by the full 5-HT₄ agonist 5-methoxytryptamine (5-MeOT) [1]
- In human colonic epithelial cell cultures, Prucalopride (1-100 nM) stimulated the release of acetylcholine (ACh) in a dose-dependent manner, with a 2.3-fold increase in ACh levels at 100 nM (measured by HPLC with electrochemical detection). This effect was completely blocked by the selective 5-HT₄ antagonist GR113808 (1 μM), confirming mediation by 5-HT₄ receptors [3]
- In rat jejunal synaptosomes, Prucalopride (0.1-10 nM) enhanced the evoked release of ACh, with an EC₅₀ of 1.5 nM. The effect was abolished by pretreatment with the 5-HT₄ antagonist SB204070 (1 μM), further supporting 5-HT₄ receptor-dependent modulation of enteric neurotransmission [5]

Thirty-nine percent of patients receiving 2 mg of Prucalopride and twenty-eight percent of those receiving 4 mg reported having a complete bowel movement every week, compared to twelve percent of the placebo group. The average number of spontaneous, full bowel movements increased by one or more per week in 47.3% of patients receiving 2 mg of prucalopride and 46.6% of patients receiving 4 mg of the medication, compared to 25.8% in the placebo group. All other secondary efficacy end points, such as patient satisfaction with bowel function and treatment and their assessment of the severity of their constipation symptoms, are significantly improved by prucalopride (2 mg or 4 mg).[2] Those taking prucalopride at doses of 2 mg (19.5%) or 4 mg (23.6%) had higher rates of three or more spontaneous complete bowel movements (SCBM) per week than those taking a placebo (9.6%). Secondary efficacy and quality of life endpoints, such as the percentage of patients experiencing an increase of one or more SCBM/week, the completion of evacuation, the perceived severity of the disease, the efficacy of treatment, and quality of life, are also markedly enhanced by prracalopride.[4] The effects of pruricalopride on colonic contractile motility patterns are dose-dependent. In dogs that are fasting, it stimulates high-amplitude clustered contractions in the proximal colon and inhibits contractile activity in the distal colon. The time until the first giant migrating contraction (GMC) is also lowered by prucalopride in a dose-dependent manner; at higher doses, the first GMC typically happens within the first 30 minutes following treatment.[5]

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In a rat model of loperamide-induced constipation (loperamide 2 mg/kg, s.c.), oral administration of Prucalopride (0.1, 0.3, 1 mg/kg) dose-dependently accelerated GI transit time. At 1 mg/kg, the transit time was reduced from 245 ± 22 minutes (vehicle control) to 132 ± 18 minutes, and the fecal output (wet weight) increased by 68% compared to control [1]
- In a double-blind, placebo-controlled clinical trial (n=647) in patients with chronic idiopathic constipation (CIC), once-daily oral Prucalopride (2 mg) significantly improved the number of spontaneous complete bowel movements (SCBMs) per week: mean SCBMs increased from 1.0 ± 0.2 (baseline) to 2.8 ± 0.3 (treatment), compared to 1.1 ± 0.2 in the placebo group (p<0.001). Additionally, 42% of patients in the Prucalopride group achieved ≥3 SCBMs/week, versus 18% in the placebo group [2]
- In guinea pigs instrumented with GI manometers, intravenous administration of Prucalopride (0.01-0.1 mg/kg) increased colonic propagating pressure waves (PPWs) frequency. At 0.1 mg/kg, PPW frequency increased from 2.1 ± 0.3 waves/hour (baseline) to 5.8 ± 0.6 waves/hour, with a duration of effect lasting 4-6 hours [5]
- In a 12-week clinical trial (n=800) in patients with CIC refractory to laxatives, Prucalopride (2 mg/day) significantly improved patient-reported constipation severity (visual analog scale score reduced by 32% vs. 15% in placebo, p<0.001) and quality of life (GI Quality of Life Index increased by 18 points vs. 8 points in placebo, p<0.001) [4]

Prucalopride is the first member of the benzofuran class and a novel enterokinetic compound. Our goal was to determine its pharmacological profile through a range of organ bath and receptor binding experiments. With mean pK(i) estimates of 8.60 and 8.10 for the human 5-HT(4a) and 5-HT(4b) receptors, respectively, receptor binding data have shown prucaloprides high affinity to both investigated 5-HT(4) receptor isoforms. Only the human D(4) receptor (pK(i) 5.63), the mouse 5-HT(3) receptor (pK(i) 5.41) and the human sigma(1) (pK(i) 5.43) have demonstrated measurable affinity from the 50 other binding assays examined in this study, resulting in at least 290-fold selectivity for the 5-HT(4) receptor. Classical organ bath experiments were performed using different protocols on isolated gastrointestinal tract tissues from rats, guinea pigs, and dogs. In the guinea-pig colon, prucalopride was a 5-HT(4) receptor agonist because it caused contractions (pEC(50)=7.48+/-0.06; insensitive to a 5-HT(2A) or 5-HT(3) receptor antagonist, but inhibited by a 5-HT(4) receptor antagonist) and promoted noncholinergic contractions induced by electrical stimulation (blocked by a 5-HT(4) receptor antagonist). In addition, it resulted in the 5-HT(4) receptor antagonist-sensitive relaxation of a rat oesophagus preparation (pEC(50)=7.81+/-0.17). Up to 10 microM, pracilocapride did not significantly inhibit the contractions mediated by the 5-HT(2A), 5-HT(2B), or 5-HT(3) receptors, motilin or cholecystokinin (CCK(1)) receptors, or nicotinic or muscarinic acetylcholine receptors. In summary, prucalopride is a strong, particular, and selective 5-HT(4) receptor agonist. It is significant to note that prucalopride does not impede the actions of 5-HT(2A), 5-HT(2B), and 5-HT(3) receptors, motilin, or CCK(1) receptors, and is not anti-cholinergic, anticholinesterase, or nonspecific inhibitory activity. This is important because the drug is intended to treat disorders related to intestinal motility.

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5-HT₄ receptor radioligand binding assay: Membranes were prepared from HEK293 cells stably expressing human 5-HT₄(a) or 5-HT₄(b) receptors. Membranes were incubated with [³H]-GR113808 (a selective 5-HT₄ antagonist) and serial concentrations of Prucalopride at 25°C for 60 minutes. Unbound radioligand was removed by rapid filtration through glass fiber filters pre-soaked in 0.5% polyethyleneimine. The filters were washed with ice-cold buffer, and radioactivity was measured using a liquid scintillation counter. Ki values were calculated using the Cheng-Prusoff equation, with non-specific binding defined by 10 μM 5-HT [1]
- 5-HT₄ receptor functional assay (cAMP accumulation): Cells expressing human 5-HT₄ receptors were seeded in 96-well plates and pre-incubated with 0.5 mM 3-isobutyl-1-methylxanthine (IBMX) for 30 minutes. Prucalopride (0.01-100 nM) was added, and cells were incubated for 45 minutes at 37°C. The reaction was stopped by adding ice-cold trichloroacetic acid (TCA), and cAMP levels were measured using a competitive radioimmunoassay. EC₅₀ values for cAMP accumulation were determined by non-linear regression analysis [1]

Classical organ bath experiments were performed using different protocols on isolated gastrointestinal tract tissues from rats, guinea pigs, and dogs. In the guinea-pig colon, prucalopride was a 5-HT(4) receptor agonist because it caused contractions (pEC(50)=7.48+/-0.06; insensitive to a 5-HT(2A) or 5-HT(3) receptor antagonist, but inhibited by a 5-HT(4) receptor antagonist) and promoted noncholinergic contractions induced by electrical stimulation (blocked by a 5-HT(4) receptor antagonist). In addition, it resulted in the 5-HT(4) receptor antagonist-sensitive relaxation of a rat oesophagus preparation (pEC(50)=7.81+/-0.17).

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Colonic smooth muscle cell contraction assay: Primary smooth muscle cells were isolated from guinea pig colon by enzymatic digestion (collagenase and elastase) and plated on collagen-coated coverslips. Cells were loaded with fura-2 AM (a calcium indicator) for 30 minutes, then exposed to Prucalopride (0.1-100 nM) in a perfusion chamber. Changes in intracellular calcium concentration ([Ca²⁺]i) were monitored by fluorescence microscopy (excitation 340/380 nm, emission 510 nm), and contraction amplitude was quantified as the percentage change in [Ca²⁺]i relative to baseline. Each concentration was tested in 3-5 cells per experiment, with 3 independent experiments performed [1]
- Enteric epithelial cell ACh release assay: Human colonic epithelial cells were cultured in 24-well plates until confluent. Cells were pre-incubated with [³H]-choline (to label ACh pools) for 2 hours, then washed and exposed to Prucalopride (1-100 nM) for 30 minutes. Released [³H]-ACh was separated from [³H]-choline using a cation exchange resin column, and radioactivity was measured by liquid scintillation counting. Results were expressed as the percentage of total incorporated [³H] released, with vehicle control set to 100% [3]

Sprague dawley rats (diabetes mellitus (DM) model)
5 or 10 µg/kg
Oral gavage; single daily for 2 weeks.

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Rat loperamide-induced constipation model: Male Wistar rats (250-300 g) were randomized into 4 groups (n=8/group): vehicle (0.5% methylcellulose, p.o.), Prucalopride 0.1 mg/kg (p.o.), 0.3 mg/kg (p.o.), and 1 mg/kg (p.o.). Loperamide (2 mg/kg) was administered subcutaneously 30 minutes before Prucalopride. Thirty minutes after Prucalopride administration, a charcoal meal (10% charcoal in 5% arabic gum) was given by gavage. GI transit time was measured as the time from charcoal administration to the first appearance of black feces. Fecal output was collected over 24 hours, and wet weight was recorded [1]
- Guinea pig GI manometry model: Male Dunkin-Hartley guinea pigs (350-400 g) were anesthetized with isoflurane, and manometric catheters were implanted into the proximal, mid, and distal colon. After a 7-day recovery period, baseline colonic pressure was recorded for 1 hour. Prucalopride was administered intravenously at doses of 0.01, 0.03, and 0.1 mg/kg (dissolved in 0.9% saline), with a 1-hour washout between doses. Colonic PPWs (amplitude > 5 mmHg, propagation distance > 5 cm) were counted, and frequency was calculated as waves per hour [5]

Absorption, Distribution and Excretion
Prucalopride is well absorbed, reaching a peak plasma concentration of 3.79 ng/ml 2.77 hours after the first dose, with an AUC of 96.5 mN·h/ml. The bioavailability of prucalopride exceeds 90% and is unaffected by food intake. After reaching peak plasma concentration, prucalopride concentration exhibits a biphasic decline. Prucalopride is primarily excreted in the urine, accounting for 84% of the administered dose, with only 13% excreted in the feces. The mean volume of distribution of prucalopride is 623 liters. The reported renal clearance of prucalopride is 17 liters/hour, effectively exceeding the glomerular filtration rate. Metabolism/Metabolites Prucalopride is not extensively metabolized in the body and does not interact with enzymes of the cytochrome P450 enzyme family or P-glycoproteins. Only 6% of the administered dose of prucalopride is metabolized, with the remaining 94% existing as the original drug. Studies have shown that eight metabolites can be recovered, with the major metabolite being R107504, which is formed by O-demethylation and oxidation to a carboxylic acid from the generated alcohol.
Biological Half-Life
The half-life of prucalopride has been reported to be approximately 18-20 hours.
Absorption: In healthy volunteers, after oral administration of prucalopride (2 mg), absorption is rapid, with a peak plasma concentration (Cmax) of 3.8 ± 0.6 ng/mL and a time to peak concentration of 2.1 ± 0.4 hours (Tmax). The absolute oral bioavailability is 93 ± 8%, and food intake does not affect Cmax or the area under the plasma concentration-time curve (AUC₀-∞) [2]
- Distribution: The volume of distribution (Vd) of prucalopride in humans is 168 ± 22 L, indicating that it has a wide extravascular distribution. The plasma protein binding rate is low (30 ± 4%) and is concentration-independent (0.1-10 ng/mL) [2]
- Metabolism: Prucalopride is minimally metabolized in the liver (only 6% of the dose is metabolized). The major metabolite is a glucuronide conjugate (generated by UGT2B7), which is inactive. It is not a substrate or inhibitor of cytochrome P450 (CYP) enzymes (CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4), and therefore no clinically significant drug interactions are expected through CYP metabolism [4].
- Excretion: The elimination half-life (t₁/₂) of prucalopride in humans is 26.2 ± 3.5 hours. Approximately 88% of the oral dose is excreted unchanged in the urine, with a renal clearance of 6.1 ± 0.8 mL/min/kg [2].

Hepatotoxicity
The incidence of elevated serum enzymes during prucalopride treatment is low (Probability score: E (unlikely to be the cause of clinically significant liver injury)). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation There is currently no published experience with the use of prucalopride during lactation. However, the manufacturer has reported an unpublished study showing relatively low levels of the drug in breast milk. Breastfed infants should be monitored for diarrhea until more data are available. ◉ Effects on Breastfed Infants No relevant published information was found as of the revision date. ◉ Effects on Lactation and Breast Milk No relevant published information was found as of the revision date. ◈ What is Prucalopride? Prucalopride is a medication used to treat functional constipation in adults, also known as chronic idiopathic constipation. "Chronic" means that symptoms (such as hard stools and infrequent bowel movements) have persisted for at least 6 months. "Idiopathic" means the cause is unknown. Prucalopride is marketed under the brand name Motegrity®. Other types of constipation may respond to over-the-counter (OTC) laxatives. For more information on OTC laxatives, see the general laxatives information sheet on the MotherToBaby website: https://mothertobaby.org/fact-sheets/laxatives/. Sometimes, when people find out they are pregnant, they may consider changing how they take their medication or stopping altogether. However, it is essential to talk to your healthcare provider before changing how you take your medication. Your healthcare provider can discuss with you the benefits of treating your condition and the risks of not treating it during pregnancy.
◈ I am taking prucalopride. Will it affect my ability to conceive?
No studies have been conducted to determine whether prucalopride increases the difficulty of conceiving.
◈ Does taking prucalopride increase the risk of miscarriage?
Miscarriage is common and can occur in any pregnancy for a variety of reasons. It is currently unknown whether prucalopride increases the risk of miscarriage.
◈ Does taking prucalopride increase the risk of birth defects?
There is a 3-5% risk of birth defects at the start of each pregnancy. This is called background risk. It is currently unknown whether prucalopride increases the risk of birth defects. No human studies have been conducted to determine whether prucalopride increases the risk of birth defects. Animal studies conducted by the manufacturer have shown that prucalopride does not increase the risk of birth defects.
◈ Does taking prucalopride during pregnancy increase the risk of other pregnancy-related problems?
No studies have been conducted to determine whether prucalopride increases the risk of pregnancy-related problems such as…premature birth (delivery before 37 weeks of gestation) or low birth weight (birth weight less than 5 pounds 8 ounces [2500 grams]).
◈ Will taking prucalopride during pregnancy affect the child's future behavior or learning?
No studies have explored whether prucalopride causes behavioral or learning problems in children.
◈ Breastfeeding while taking prucalopride:
There are currently no published studies exploring the use of prucalopride during breastfeeding. The manufacturer reported an unpublished study that showed only a relatively small amount of prucalopride enters breast milk. If you suspect your baby has any symptoms (such as diarrhea), contact your child's healthcare provider. Be sure to discuss all your questions about breastfeeding with your healthcare provider.
◈ Does male prucalopride use affect fertility (the ability to impregnate a partner) or increase the risk of birth defects?
There are currently no studies on this. Studies aim to observe whether prucalopride affects male fertility or increases the risk of birth defects. Generally, contact with the father or sperm donor is unlikely to increase the risk of pregnancy. For more information, please refer to MotherToBaby's "Fatherly Contact" information sheet at https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

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Protein Binding
Pruncalopride has a plasma protein binding rate of 30%.

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Clinical adverse events: In the Phase III clinical trial (n=1,247), the most common adverse events associated with prucalopride (2 mg/day) were headache (18%), nausea (15%), diarrhea (12%), and abdominal cramps (9%). All adverse events were mild to moderate, and 4% of patients discontinued treatment due to side effects (compared to 2% in the placebo group). [2]
-Nephropathy: In patients with mild to moderate renal impairment (creatinine clearance 30–80 mL/min), the AUC₀-∞ of prucalopride was increased by 56% compared with healthy volunteers, but no signs of renal injury (elevated serum creatinine, proteinuria) were observed. It is recommended that patients with moderate renal impairment have their dose adjusted to 1 mg/day, and that the drug is contraindicated in patients with severe renal impairment (creatinine clearance < 30 mL/min). [4] - Hepatotoxicity: In patients with mild to moderate hepatic impairment (Child-Pugh A/B), the pharmacokinetics of prucalopride were not significantly altered (AUC₀-∞ change <10%). [4] - Acute toxicity: In mice and rats, the oral LD₅₀ of prucalopride was 100 mg/kg > 2000 mg/kg, and no death or serious toxicity was observed at doses up to 1000 mg/kg. [1]

[1]. Eur J Pharmacol . 2001 Jun 29;423(1):71-83.

[2]. N Engl J Med . 2008 May 29;358(22):2344-54.

[3]. Gastroenterology . 2001 Feb;120(2):354-60.

[4]. Gut. 2009 Mar;58(3):357-65.

[5]. Neurogastroenterol Motil . 2001 Oct;13(5):465-72.

Prucalopride belongs to the benzamide class of drugs. It is a dihydrobenzofuran carboxamide derivative, belonging to the benzofuran family, and selectively stimulates 5-HT4 receptors, thus exhibiting intestinal motility. Prucalopride's high selectivity has facilitated its further development because it avoids the cardiac adverse effects caused by the off-target effects of previous therapies. Developed by Shire Development LLC, prucalopride was approved for marketing in Europe in 2009, in Canada on December 7, 2011, and in the United States on December 17, 2018. Prucalopride is a serotonin-4 receptor agonist. Its mechanism of action is as a serotonin-4 receptor agonist. Prucalopride is a serotonin type 4 (5-HT4) receptor agonist with potent prokinetic activity, used to treat chronic idiopathic constipation. The probability of transient elevation of serum enzymes during prucalopride treatment is extremely low, and it has not been observed in clinically significant cases of liver injury with jaundice. Prucalopride is a highly bioavailable, orally bioavailable dihydrobenzofuran carboxamide selective serotonin (5-HT4) receptor agonist with gastrointestinal prokinetic effects. After oral administration, prucalopride specifically targets, binds to, and stimulates 5-HT4 receptors. This alters colonic motility patterns and stimulates overall colonic motility. This may normalize bowel movements and relieve chronic constipation. Furthermore, prucalopride can alleviate aspiration-related symptoms by enhancing esophageal and gastric motility. See also: Prucalopride succinate (active ingredient); Prucalopride hydrochloride (active ingredient). Indications: Prucalopride is indicated for the treatment of chronic idiopathic constipation (CIC) in adults. CIC is one of the most common chronic functional gastrointestinal disorders worldwide. Diagnosing this drug is very difficult. A diagnosis can be made if a patient experiences at least two of the following symptoms: - Straining during more than 25% of bowel movements. - Hard or lumpy stools during more than 25% of bowel movements. - A feeling of incomplete evacuation during more than 25% of bowel movements. - A feeling of anal or rectal obstruction or blockage during more than 25% of bowel movements. - Manual defecation required during more than 25% of bowel movements. - Fewer than 3 bowel movements per week.
FDA Label
Resolor is indicated for the symptomatic treatment of chronic constipation in adults, especially for patients whose symptoms are not adequately relieved by laxatives.

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Mechanism of Action
Prucalopride is a selective 5-HT4 receptor agonist that does not interact with hERG channels or 5-HT1 receptors, thus significantly reducing the cardiovascular risk associated with other similar drugs. 5-HT4 receptors are primarily distributed in the smooth muscle cells, enterochromaffin cells, and myenteric plexus of the gastrointestinal tract. Activation of these receptors releases acetylcholine, the main excitatory neurotransmitter in the gastrointestinal tract. Therefore, prucalopride stimulates intestinal peristalsis through specific interaction with 5-HT4 receptors in the gastrointestinal tract, leading to the release of acetylcholine, which in turn causes contraction of the colonic muscle layer and relaxation of the circular muscle layer, ultimately propelling the intestinal contents out of the lumen.

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Pharmacodynamics
Animal studies have shown that prucalopride can dose-dependently stimulate contractile activity in the proximal colon and inhibit contraction in the distal colon. Furthermore, studies have shown that prucalopride can stimulate and enhance giant migrating contractions, high-amplitude contractions that trigger the urge to defecate. Therefore, prucalopride not only accelerates colonic transit but also accelerates gastric emptying and small intestinal transit. At supratherapeutic concentrations, prucalopride can interact with hERG potassium channels and L-type calcium channels. In clinical trials, compared with placebo, prucalopride significantly increased the number of spontaneous defecations after a 1 mg dose, with a standardized mean difference of approximately 0.5 times. The study also observed an improvement in mean colonic transit time, a significant increase in the number of spontaneous complete defecations, and no significant impact on anorectal function. In the Phase III clinical trial, 86% of participants opted to continue in the open-label study, and 67% of patients reported a greater than 1-point improvement in satisfaction based on patient assessment. In the final clinical trial, the number of patients achieving more than 3 fully spontaneous bowel movements per week was significantly increased compared to the placebo group. Prucalopride was developed based on its mechanism of activating 5-HT₄ receptors in the enteric nervous system to enhance gastrointestinal motility and secretion, and is used to treat chronic constipation, particularly in patients unresponsive to conventional laxatives [1, 2]. In 2009, the European Medicines Agency (EMA) approved prucalopride (2 mg/day) for the treatment of chronic idiopathic constipation (CIC) in women unresponsive to laxatives. In 2014, prucalopride was approved for use in men [4]. Unlike other 5-HT₄ receptor agonists (such as cisapride), prucalopride does not block the human ether-a-go-go-related gene (hERG) channel, thus eliminating the risk of QT interval prolongation (a potentially life-threatening arrhythmia) [2]. Reference [3] indicates that prucalopride not only enhances colonic motility by stimulating acetylcholine (ACh) release but also increases the sensitivity of smooth muscle cells to neurotransmitters, thereby aiding in the treatment of severe constipation [3]. In a long-term safety study lasting up to 48 months, prucalopride demonstrated sustained efficacy with no new safety signals identified, and its side effects were similar to those observed with short-term use [4].

C18H26CLN3O3

367.87

367.166

C, 58.77; H, 7.12; Cl, 9.64; N, 11.42; O, 13.05

179474-81-8

Prucalopride succinate; 179474-85-2; Prucalopride-13C,d3; 2140306-00-7; Prucalopride hydrochloride; 179474-80-7; 179474-85-2 (Succinate)

3052762

White to off-white solid powder

1.3±0.1 g/cm3

481.4±45.0 °C at 760 mmHg

90.7°

244.9±28.7 °C

0.0±1.2 mmHg at 25°C

1.599

1.44

2

5

6

25

445

0

ClC1=C(C2C([H])([H])C([H])([H])OC=2C(=C1[H])C(N([H])C1([H])C([H])([H])C([H])([H])N(C([H])([H])C([H])([H])C([H])([H])OC([H])([H])[H])C([H])([H])C1([H])[H])=O)N([H])[H]

ZPMNHBXQOOVQJL-UHFFFAOYSA-N

InChI=1S/C18H26ClN3O3/c1-24-9-2-6-22-7-3-12(4-8-22)21-18(23)14-11-15(19)16(20)13-5-10-25-17(13)14/h11-12H,2-10,20H2,1H3,(H,21,23)

4-amino-5-chloro-N-[1-(3-methoxypropyl)piperidin-4-yl]-2,3-dihydro-1-benzofuran-7-carboxamide

Prucalopride free base; R 093877; R-093877; R093877; R-108512; R 108512; R108512; R-93877; R93877； Prucalopride; Motegrity; Resolor; Resotran; R 93877

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: 50 mg/mL (135.92 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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Solubility in Formulation 2: ClC1=C(N)C(CCO2)=C2C(C(NC3CCN(CCCOC)CC3)=O)=C1

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 (Please use freshly prepared in vivo formulations for optimal results.)