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ralfinamide  (Newron Pharmaceuticals SpA)

 
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    Newron Pharmaceuticals SpA ralfinamide
    Ralfinamide, supplied by Newron Pharmaceuticals SpA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ralfinamide/ralfinamide/pm40403415-278-9-18
    Average 90 stars, based on 1 article reviews
    ralfinamide - by Bioz Stars, 2026-10
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    other:

    Article Title: Synthesis and Evaluation of Novel α-Aminoamides Containing an Indole Moiety for the Treatment of Neuropathic Pain
    Article Snippet: Ralfinamide is an orally active selective blocker of the VGSC, Nav1.7, and has been developed by Newron Pharmaceuticals [5].

    Article Title: Synthesis and Evaluation of Novel α-Aminoamides Containing an Indole Moiety for the Treatment of Neuropathic Pain
    Article Snippet: Ralfinamide is an orally active selective blocker of the VGSC, Nav1.7, and has been developed by Newron Pharmaceuticals [ ].

    Article Title: Advances in targeting voltage-gated sodium channels with small molecules.
    Article Snippet: DOI: 10.1002/cmdc.201200298

    Clinical Proteomics:

    Article Title: Effects of ralfinamide in models of nerve injury and chemotherapy-induced neuropathic pain.
    Article Snippet: Neuropathic pain is among the most common and difficult-to-treat types of chronic pain and is associated with sodium channel malfunction.. The sodium channel blocker ralfinamide has exhibited potent analgesic effects in several preclinical pain models and in patients with mixed neuropathic pain syndromes (Phase II trials), but it failed to ameliorate neuropathic low back pain in Phase III trials.. It is unclear whether ralfinamide is effective against neuropathic pain induced by specified etiologies.



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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
    Ralfinamide, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ralfinamide/Ralfinamide/pm34103689-48-0-4
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    ralfinamide  (Newron Pharmaceuticals SpA)
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
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    ralfinamide nw-1029  (Newron Pharmaceuticals SpA)
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
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    medchemexpress llc  (MedChemExpress)
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
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    sodium/chloride channel inhibitor ralfinamide  (Tocris)
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.
    Sodium/Chloride Channel Inhibitor Ralfinamide, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.

    Journal: Acta pharmacologica Sinica

    Article Title: Inhibition of Nav1.7 channel by a novel blocker QLS-81 for alleviation of neuropathic pain.

    doi: 10.1038/s41401-021-00682-9

    Figure Lengend Snippet: Fig. 1 Concentration-dependent inhibition of Nav1.7 currents expressed in HEK293 cells by compound QLS-81. a Chemical structure of QLS-81: (S)-2-((3-(4-((2-fluorobenzyl) oxy) phenyl) propyl) amino) propanamide and ralfinamide. b Left panel, top, Nav1.7 currents stably expressed in HEK293 cells held at −130 mV were elicited by a double-pulse protocol consisting of a conditional pulse at 0 mV (15 ms) for channel activation and a test pulse at 0 mV (15 ms) for 50% channel inactivation. Left panel, bottom, representative current traces elicited by the second test pulse before and after application of QLS-81. The dashed line represents zero-current levels. Right panel, summary for normalized inhibition of activated and inactivated Nav1.7 currents by QLS-81. Paired t-test, ***P < 0.001, n = 10. c Inhibition of representative Nav1.7 current traces elicited by the test pulse (panel (b)) before and after QLS-81 (left panel) and ralfinamide (middle panel) at different concentrations. The dashed line represents zero-current levels. Right panel, curves were fitted using a logistic function for concentration- dependent inhibition of Nav1.7 by QLS-81 (black) with IC50 of 3.5 ± 1.5 μM (n = 3–11) and ralfinamide (red) with IC50 of 37.1 ± 2.9 μM (n = 5–8). d Representative current traces of Nav1.4 (left panel) and Nav1.5 (middle panel) elicited by the depolarizing potential at 0 mV (test pulse of a panel (b)) before and after different concentrations of QLS-81. The dashed line represents zero-current levels. Right panel, curves were fitted using the logistic function for concentration-dependent inhibition of Nav1.4 with IC50 of 37.3 ± 7.3 μM (n = 5) and Nav1.5 with 15.4 ± 1.6 μM (n = 5–8) by QLS-81. All data were expressed as the mean ± SEM.

    Article Snippet: Ralfinamide was purchased from MedChemExpress LLC.

    Techniques: Concentration Assay, Inhibition, Stable Transfection, Activation Assay

    Fig. 5 Antinociceptive effects of QLS-81 on pain induced by spinal nerve injury (SNI) and inflammation in mice. a Top panel, a schematic time-course of paw mechanical withdrawal threshold (PMWT) measured by von Frey hair stimulation in a mouse model of SNI. Bottom panel, dose-dependent antinociception by QLS-81 (2, 5, and 10 mg/kg, i.p.), morphine (5 mg/kg), and ralfinamide (10 mg/kg) in SNI model. Two-way ANOVA followed by Bonferroni post hoc tests revealed a significant decrease of PMWT between-group sham and group vehicle, ***P < 0.001; a significant increase of PMWT in QLS-81 (2, 5, 10 mg/kg, i.p.) injected groups, compared with group vehicle, ##P < 0.01, ###P < 0.001; and also a significant difference between group QLS-81 (10 mg/kg) and group ralfinamide (10 mg/kg), $$$P < 0.001. All data were expressed as the mean ± SEM, n = 10–12. b Top panel, experimental design, and schedule for formalin test in a mouse model of inflammatory pain. Bottom panels, formalin-induced spontaneous pain behavior was divided into two phases and analyzed following subcutaneous (sc.) injection of formalin. QLS-81 (5, 10, and 20 mg/kg) dose-dependently attenuated the nocifensive behaviors induced by formalin at phase II (right) but not at phase I. One-way ANOVA followed by Tukey test, *P < 0.01 and ***P < 0.001 vs. vehicle, n = 10–12. All data were expressed as the mean ± SEM.

    Journal: Acta pharmacologica Sinica

    Article Title: Inhibition of Nav1.7 channel by a novel blocker QLS-81 for alleviation of neuropathic pain.

    doi: 10.1038/s41401-021-00682-9

    Figure Lengend Snippet: Fig. 5 Antinociceptive effects of QLS-81 on pain induced by spinal nerve injury (SNI) and inflammation in mice. a Top panel, a schematic time-course of paw mechanical withdrawal threshold (PMWT) measured by von Frey hair stimulation in a mouse model of SNI. Bottom panel, dose-dependent antinociception by QLS-81 (2, 5, and 10 mg/kg, i.p.), morphine (5 mg/kg), and ralfinamide (10 mg/kg) in SNI model. Two-way ANOVA followed by Bonferroni post hoc tests revealed a significant decrease of PMWT between-group sham and group vehicle, ***P < 0.001; a significant increase of PMWT in QLS-81 (2, 5, 10 mg/kg, i.p.) injected groups, compared with group vehicle, ##P < 0.01, ###P < 0.001; and also a significant difference between group QLS-81 (10 mg/kg) and group ralfinamide (10 mg/kg), $$$P < 0.001. All data were expressed as the mean ± SEM, n = 10–12. b Top panel, experimental design, and schedule for formalin test in a mouse model of inflammatory pain. Bottom panels, formalin-induced spontaneous pain behavior was divided into two phases and analyzed following subcutaneous (sc.) injection of formalin. QLS-81 (5, 10, and 20 mg/kg) dose-dependently attenuated the nocifensive behaviors induced by formalin at phase II (right) but not at phase I. One-way ANOVA followed by Tukey test, *P < 0.01 and ***P < 0.001 vs. vehicle, n = 10–12. All data were expressed as the mean ± SEM.

    Article Snippet: Ralfinamide was purchased from MedChemExpress LLC.

    Techniques: Injection