Ropivacaine inhibits the pressure-induced increase in filtration coefficient (Kf) without affecting pulmonary artery pressure (Ppa), pulmonary capillary pressure (Ppc), and dispersion characteristics (ZC) [2]. Ropivacaine prevents PaO2, lung wet-to-dry ratio, and choroidal volume from maintaining at pseudo-waveform levels demonstrating pressure-induced pulmonary edema and associated hyperpermeability [2]. Ropivacaine blocks pressure-induced pulmonary edema in lung nitro compared with choroidal lung

Animal/Disease Models: Adult SD (SD (Sprague-Dawley)) rat (300–400g) [1]
Doses: 1 μM
Route of Administration: Infusion (added to in the perfusate reservoir)
Experimental Results:diminished pressure dependence. The filter coefficient (Kf) increases.

Absorption, Distribution and Excretion
Ropivacaine pharmacokinetics are highly dependent on the dose, route of administration, and patient condition. Following epidural administration ropivacaine undergoes complete and biphasic absorption.
Following intravenous administration, 86% of the administered dose of ropivacaine is excreted in the urine, 1% of which comprises unchanged parent drug.
Following intravascular infusion, ropivacaine has a steady-state volume of distribution of 41 ± 7 liters. Ropivacaine is able to readily cross the placenta.
Following intravenous administration, ropivacaine has a mean plasma clearance of 387 ± 107 mL/min, an unbound plasma clearance of 7.2 ± 1.6 L/min, and a renal clearance of 1 mL/min.

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Metabolism / Metabolites
Ropivacaine undergoes extensive metabolism, primarily via CYP1A2-mediated aromatic hydroxylation to 3-OH-ropivacaine. The main metabolites excreted in the urine are the N-dealkylated metabolite (PPX) and 3-OH-ropivacaine. Other identified metabolites include 4-OH-ropivacaine, the 3-hydroxy-N-dealkylated (3-OH-PPX) and 4-hydroxy-N-dealkylated (4-OH-PPX) metabolites, and 2-hydroxy-methyl-ropivacaine (which has been identified but not quantified). Unbound PPX, 3-hydroxy-, and 4-hydroxy-ropivacaine have demonstrated pharmacological activity in animal models less than that of ropivacaine.
Ropivacaine has known human metabolites that include PPX and 3-hydroxy-ropivacaine.
Hepatic
Route of Elimination: Ropivacaine is extensively metabolized in the liver, predominantly by aromatic hydroxylation mediated by cytochrome P4501A to 3-hydroxy ropivacaine. After a single IV dose approximately 37% of the total dose is excreted in the urine as both free and conjugated 3-hydroxy ropivacaine. In total, 86% of the ropivacaine dose is excreted in the urine after intravenous administration of which only 1% relates to unchanged drug.
Half Life: Approximately 4.2 hours.

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Biological Half-Life
The mean terminal half-life of ropivacaine is 1.8 ± 0.7 hours after intravascular administration and 4.2 ± 1 hour after epidural administration.

Toxicity Summary
Local anesthetics such as Ropivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Specifically, they block the sodium-channel and decrease chances of depolarization and consequent action potentials. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers.

[1]. Ropivacaine: a review of its use in regional anaesthesia and acute pain management. Drugs. 2005;65(18):2675-717.

[2]. Epidural sustained release ropivacaine prolongs anti-allodynia and anti-hyperalgesia in developing and established neuropathic pain. PLoS One. 2015 Jan 24;10(1):e0117321.

[3]. The inhibitory effects of bupivacaine, levobupivacaine, and ropivacaine on K2P (two-pore domain potassium) channel TREK-1. J Anesth.

[4]. Ropivacaine Inhibits Pressure-Induced Lung Endothelial Hyperpermeability in Models of Acute Hypertension. Life Sci. 2019 Apr 1;222:22-28.

(S)-ropivacaine is a piperidinecarboxamide-based amide-type local anaesthetic (amide caine) in which (S)-N-propylpipecolic acid and 2,6-dimethylaniline are combined to form the amide bond. It has a role as a local anaesthetic. It is a piperidinecarboxamide and a ropivacaine.
Ropivacaine is an aminoamide local anesthetic drug marketed by AstraZeneca under the trade name Naropin. It exists as a racemate of its S- and R-enantiomers, although the marketed form is supplied only as the purified S-enantiomer.
Ropivacaine is an Amide Local Anesthetic. The physiologic effect of ropivacaine is by means of Local Anesthesia.
Ropivacaine is only found in individuals that have used or taken this drug. It is a local anaesthetic drug belonging to the amino amide group. The name ropivacaine refers to both the racemate and the marketed S-enantiomer. Ropivacaine hydrochloride is commonly marketed by AstraZeneca under the trade name Naropin. Local anesthetics such as Ropivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Specifically, they block the sodium-channel and decrease chances of depolarization and consequent action potentials. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers.
An anilide used as a long-acting local anesthetic. It has a differential blocking effect on sensory and motor neurons.

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Drug Indication
Ropivacaine is indicated in adult patients for the induction of regional or local anesthesia for surgery or acute pain management.

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Mechanism of Action
Local anesthetics like ropivacaine block the generation and conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Specifically, they block the sodium channel and decrease chances of depolarization and consequent action potentials. In general, the progression of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers.

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Pharmacodynamics
In contrast to most other local anesthetics, the presence of [epinephrine] does not affect the time of onset, duration of action, or the systemic absorption of ropivacaine.

C17H26N2O

274.4

274.204

84057-95-4

Ropivacaine hydrochloride monohydrate;132112-35-7;Ropivacaine hydrochloride;98717-15-8;Ropivacaine-d7 hydrochloride;1217667-10-1;Ropivacaine mesylate;854056-07-8;Ropivacaine-d7;684647-62-9;(Rac)-Ropivacaine-d7;1392208-04-6

175805

White to off-white solid powder

1.0±0.1 g/cm3

410.2±45.0 °C at 760 mmHg

144 - 146ºC

201.9±28.7 °C

0.0±1.0 mmHg at 25°C

1.552

3.11

1

2

4

20

308

1

CCCN1CCCC[C@H]1C(=O)NC2=C(C=CC=C2C)C

ZKMNUMMKYBVTFN-HNNXBMFYSA-N

InChI=1S/C17H26N2O/c1-4-11-19-12-6-5-10-15(19)17(20)18-16-13(2)8-7-9-14(16)3/h7-9,15H,4-6,10-12H2,1-3H3,(H,18,20)/t15-/m0/s1

(2S)-N-(2,6-dimethylphenyl)-1-propylpiperidine-2-carboxamide

Ropivacaine Noropine Narop Ropivacainum LEA 103 Ropivacaina

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)

DMSO : ~12.5 mg/mL (~45.55 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (9.11 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (9.11 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (9.11 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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