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Valiant Co Ltd ivermectin
(A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with <t>ivermectin</t> (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
Ivermectin, supplied by Valiant Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Deep phenotypic profiling uncovers cryptic effects of antifilarial drugs"

Article Title: Deep phenotypic profiling uncovers cryptic effects of antifilarial drugs

Journal: bioRxiv

doi: 10.64898/2026.02.12.705610

(A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with ivermectin (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
Figure Legend Snippet: (A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with ivermectin (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Techniques Used: Clinical Proteomics, CellTox Assay, Fluorescence, Staining, Control

(A) Schematic showing methodology and timeline for mf temperature shift assay. (B) Mean motility, scaled to DMSO 1 hour values of B. pahangi mf at 37℃ (left panel) and room temperature (RT, right panel) across time and ivermectin (IVM) or control treatment concentrations (color-coded). P-values represent statistical differences in mf motility between DMSO and drug treatments at matched time points and temperature and were calculated using Anova/Tukey post-test and significance reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least six technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
Figure Legend Snippet: (A) Schematic showing methodology and timeline for mf temperature shift assay. (B) Mean motility, scaled to DMSO 1 hour values of B. pahangi mf at 37℃ (left panel) and room temperature (RT, right panel) across time and ivermectin (IVM) or control treatment concentrations (color-coded). P-values represent statistical differences in mf motility between DMSO and drug treatments at matched time points and temperature and were calculated using Anova/Tukey post-test and significance reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least six technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Techniques Used: Shift Assay, Control

(A) Schematic depicting the salt assay methodology and timeline. (B) Top two bar graph panels indicate combinations of KPO 4 concentrations (10mM, 25mM, 50mM, and 100mM) and NaCl concentrations (25mM, 50mM, 100mM, 125mM, and 150mM) across the remaining figure panels at vertically aligned positions. The bottom panel shows DMSO-treated B. pahangi mf motility in the presence of different concentrations of NaCl and KPO 4 across time points. (C) The top and bottom panels show optical flow differences between DMSO and ivermectin (IVM) treated B. pahangi mf (delta motility) at varying salt combinations in the presence of 50nM (top panel) or 500nM (bottom panel) IVM. P-values representing statistical differences in mf motility between DMSO and IVM treatments were calculated using Anova/Tukey post-test and significance is reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least two technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
Figure Legend Snippet: (A) Schematic depicting the salt assay methodology and timeline. (B) Top two bar graph panels indicate combinations of KPO 4 concentrations (10mM, 25mM, 50mM, and 100mM) and NaCl concentrations (25mM, 50mM, 100mM, 125mM, and 150mM) across the remaining figure panels at vertically aligned positions. The bottom panel shows DMSO-treated B. pahangi mf motility in the presence of different concentrations of NaCl and KPO 4 across time points. (C) The top and bottom panels show optical flow differences between DMSO and ivermectin (IVM) treated B. pahangi mf (delta motility) at varying salt combinations in the presence of 50nM (top panel) or 500nM (bottom panel) IVM. P-values representing statistical differences in mf motility between DMSO and IVM treatments were calculated using Anova/Tukey post-test and significance is reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least two technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Techniques Used:



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Data were obtained from 54 cells across 28 rats (Responders: n=20 cells/[8] rats; Non-responders: n=21 cells/[9] rats; Mild Responders: n=7 cells/[5] rats; Naïve: n=6 cells/[4] rats). Dose-response effects (1, 5, 10 μM; averaged over 12 min) in responders versus non-responders: ( A ) Frequency, significantly increased only in responders at 10 μM (*P = 0.0263). ( B ) Amplitude, significantly decreased only in responders at 10 μM (**P = 0.0034). ( C ) Rise time, significantly increased in non-responders at all doses (**P < 0.05 to ***P < 0.01) and in responders at 5 μM and 10 μM (*P < 0.05). ( D ) Decay time, significantly increased only in non-responders at 10 μM (*P = 0.0420). Effects at 10 μM across all groups (ethanol-naïve controls, non-responders, mild responders, responders): ( E ) Frequency, significantly increased only in responders (*P = 0.0263). ( F ) Amplitude, significantly decreased only in responders (**P = 0.0034). ( G ) Rise time, significantly increased in non-responders (*P = 0.0328) and responders (*P = 0.0467). ( H ) Decay time, significantly increased only in non-responders (*P = 0.0420). Temporal dynamics at 10 μM: ( I ) Representative sIPSC traces shown for non-responders, mild responders, and responders. ( J ) Timeline of frequency changes (3-min bins), with two-way ANOVA showing a significant time × group interaction (P < 0.0001); Bonferroni’s post-hoc tests indicated differences at 9 minutes and 12 minutes (*P < 0.05 vs non-responders and # P < 0.05 vs mild responders). ( K ) Frequency per bin relative to baseline for each group, with significant elevations in non-responders at 3 minutes (*P = 0.0150), mild responders at 6 minutes (*P = 0.0281), and responders at 9 minutes (*P = 0.0120) and 12 minutes (**P = 0.0080). All data are presented as mean ± SEM (normalized to baseline [100%]); statistical analyses used one-sample t-tests against 100% unless otherwise noted.
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Data were obtained from 54 cells across 28 rats (Responders: n=20 cells/[8] rats; Non-responders: n=21 cells/[9] rats; Mild Responders: n=7 cells/[5] rats; Naïve: n=6 cells/[4] rats). Dose-response effects (1, 5, 10 μM; averaged over 12 min) in responders versus non-responders: ( A ) Frequency, significantly increased only in responders at 10 μM (*P = 0.0263). ( B ) Amplitude, significantly decreased only in responders at 10 μM (**P = 0.0034). ( C ) Rise time, significantly increased in non-responders at all doses (**P < 0.05 to ***P < 0.01) and in responders at 5 μM and 10 μM (*P < 0.05). ( D ) Decay time, significantly increased only in non-responders at 10 μM (*P = 0.0420). Effects at 10 μM across all groups (ethanol-naïve controls, non-responders, mild responders, responders): ( E ) Frequency, significantly increased only in responders (*P = 0.0263). ( F ) Amplitude, significantly decreased only in responders (**P = 0.0034). ( G ) Rise time, significantly increased in non-responders (*P = 0.0328) and responders (*P = 0.0467). ( H ) Decay time, significantly increased only in non-responders (*P = 0.0420). Temporal dynamics at 10 μM: ( I ) Representative sIPSC traces shown for non-responders, mild responders, and responders. ( J ) Timeline of frequency changes (3-min bins), with two-way ANOVA showing a significant time × group interaction (P < 0.0001); Bonferroni’s post-hoc tests indicated differences at 9 minutes and 12 minutes (*P < 0.05 vs non-responders and # P < 0.05 vs mild responders). ( K ) Frequency per bin relative to baseline for each group, with significant elevations in non-responders at 3 minutes (*P = 0.0150), mild responders at 6 minutes (*P = 0.0281), and responders at 9 minutes (*P = 0.0120) and 12 minutes (**P = 0.0080). All data are presented as mean ± SEM (normalized to baseline [100%]); statistical analyses used one-sample t-tests against 100% unless otherwise noted.
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(A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with <t>ivermectin</t> (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
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(A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with <t>ivermectin</t> (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).
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Data were obtained from 54 cells across 28 rats (Responders: n=20 cells/[8] rats; Non-responders: n=21 cells/[9] rats; Mild Responders: n=7 cells/[5] rats; Naïve: n=6 cells/[4] rats). Dose-response effects (1, 5, 10 μM; averaged over 12 min) in responders versus non-responders: ( A ) Frequency, significantly increased only in responders at 10 μM (*P = 0.0263). ( B ) Amplitude, significantly decreased only in responders at 10 μM (**P = 0.0034). ( C ) Rise time, significantly increased in non-responders at all doses (**P < 0.05 to ***P < 0.01) and in responders at 5 μM and 10 μM (*P < 0.05). ( D ) Decay time, significantly increased only in non-responders at 10 μM (*P = 0.0420). Effects at 10 μM across all groups (ethanol-naïve controls, non-responders, mild responders, responders): ( E ) Frequency, significantly increased only in responders (*P = 0.0263). ( F ) Amplitude, significantly decreased only in responders (**P = 0.0034). ( G ) Rise time, significantly increased in non-responders (*P = 0.0328) and responders (*P = 0.0467). ( H ) Decay time, significantly increased only in non-responders (*P = 0.0420). Temporal dynamics at 10 μM: ( I ) Representative sIPSC traces shown for non-responders, mild responders, and responders. ( J ) Timeline of frequency changes (3-min bins), with two-way ANOVA showing a significant time × group interaction (P < 0.0001); Bonferroni’s post-hoc tests indicated differences at 9 minutes and 12 minutes (*P < 0.05 vs non-responders and # P < 0.05 vs mild responders). ( K ) Frequency per bin relative to baseline for each group, with significant elevations in non-responders at 3 minutes (*P = 0.0150), mild responders at 6 minutes (*P = 0.0281), and responders at 9 minutes (*P = 0.0120) and 12 minutes (**P = 0.0080). All data are presented as mean ± SEM (normalized to baseline [100%]); statistical analyses used one-sample t-tests against 100% unless otherwise noted.

Journal: Neuropharmacology

Article Title: Ivermectin Reduces Withdrawal-Induced Alcohol Intake in Rats: Association with CeA GABAergic Enhancement and P2rx4 Genetic Liability

doi: 10.1016/j.neuropharm.2026.110881

Figure Lengend Snippet: Data were obtained from 54 cells across 28 rats (Responders: n=20 cells/[8] rats; Non-responders: n=21 cells/[9] rats; Mild Responders: n=7 cells/[5] rats; Naïve: n=6 cells/[4] rats). Dose-response effects (1, 5, 10 μM; averaged over 12 min) in responders versus non-responders: ( A ) Frequency, significantly increased only in responders at 10 μM (*P = 0.0263). ( B ) Amplitude, significantly decreased only in responders at 10 μM (**P = 0.0034). ( C ) Rise time, significantly increased in non-responders at all doses (**P < 0.05 to ***P < 0.01) and in responders at 5 μM and 10 μM (*P < 0.05). ( D ) Decay time, significantly increased only in non-responders at 10 μM (*P = 0.0420). Effects at 10 μM across all groups (ethanol-naïve controls, non-responders, mild responders, responders): ( E ) Frequency, significantly increased only in responders (*P = 0.0263). ( F ) Amplitude, significantly decreased only in responders (**P = 0.0034). ( G ) Rise time, significantly increased in non-responders (*P = 0.0328) and responders (*P = 0.0467). ( H ) Decay time, significantly increased only in non-responders (*P = 0.0420). Temporal dynamics at 10 μM: ( I ) Representative sIPSC traces shown for non-responders, mild responders, and responders. ( J ) Timeline of frequency changes (3-min bins), with two-way ANOVA showing a significant time × group interaction (P < 0.0001); Bonferroni’s post-hoc tests indicated differences at 9 minutes and 12 minutes (*P < 0.05 vs non-responders and # P < 0.05 vs mild responders). ( K ) Frequency per bin relative to baseline for each group, with significant elevations in non-responders at 3 minutes (*P = 0.0150), mild responders at 6 minutes (*P = 0.0281), and responders at 9 minutes (*P = 0.0120) and 12 minutes (**P = 0.0080). All data are presented as mean ± SEM (normalized to baseline [100%]); statistical analyses used one-sample t-tests against 100% unless otherwise noted.

Article Snippet: Ivermectin (MedChemExpress, Monmouth Junction, NJ, USA) was freshly dissolved in a vehicle containing 95% physiological saline (0.9% NaCl) and 5% Tween 80 and administered intraperitoneally (i.p.) 4 hours before behavioral testing, using a Latin Square design.

Techniques:

Ethanol escalation and reduction by ivermectin. Data depict a cohort of n=32 (16 males, blue circles; 16 females, pink circles) tested in a Latin square design. ( A ) Temporal profile of operant ethanol intake (10% v/v; 0.1 mL/reinforcer). Highlighting indicates post-vapor sessions. ANOVA showed a main effect of time (P<0.0001); Bonferroni’s post-hocs revealed increases from the last pre-vapor session (session 10) to post-vapor sessions 17–22 (**P<0.01, *P<0.001). ( B ) Average intake during the final three pre-vapor vs. post-vapor sessions (paired t-test: P<0.0001). ( C ) Blood alcohol levels (BALs) across vapor weeks (Time effect: **P=0.0056); progressive increases observed from week 5 vs. weeks 6–10 (P<0.0001). ( D ) Dose-dependent reduction of ethanol intake by ivermectin (0–10 mg/kg, i.p., administered −4 h). ANOVA showed a significant treatment effect (P=0.0002); post-hocs confirmed reductions at 5 and 10 mg/kg vs. vehicle (P<0.01). ( E ) Number of rewards earned (Treatment effect: P=0.0078; * P<0.05 vs. vehicle at 5 and 10 mg/kg). ( F ) Water rewards (non-specific control) were unaffected (P=0.57). ( G ) Ethanol intake separated by sex. Two-way ANOVA showed main effects of dose (P=0.0001) and sex (P=0.0011) but no interaction. ( H ) Males only: significant treatment effect (P=0.0073; * P<0.05 at 5 and 10 mg/kg). ( I ) Females only: significant treatment effect (P=0.0279; * P<0.05 at 10 mg/kg). Data expressed as mean ± SEM.

Journal: Neuropharmacology

Article Title: Ivermectin Reduces Withdrawal-Induced Alcohol Intake in Rats: Association with CeA GABAergic Enhancement and P2rx4 Genetic Liability

doi: 10.1016/j.neuropharm.2026.110881

Figure Lengend Snippet: Ethanol escalation and reduction by ivermectin. Data depict a cohort of n=32 (16 males, blue circles; 16 females, pink circles) tested in a Latin square design. ( A ) Temporal profile of operant ethanol intake (10% v/v; 0.1 mL/reinforcer). Highlighting indicates post-vapor sessions. ANOVA showed a main effect of time (P<0.0001); Bonferroni’s post-hocs revealed increases from the last pre-vapor session (session 10) to post-vapor sessions 17–22 (**P<0.01, *P<0.001). ( B ) Average intake during the final three pre-vapor vs. post-vapor sessions (paired t-test: P<0.0001). ( C ) Blood alcohol levels (BALs) across vapor weeks (Time effect: **P=0.0056); progressive increases observed from week 5 vs. weeks 6–10 (P<0.0001). ( D ) Dose-dependent reduction of ethanol intake by ivermectin (0–10 mg/kg, i.p., administered −4 h). ANOVA showed a significant treatment effect (P=0.0002); post-hocs confirmed reductions at 5 and 10 mg/kg vs. vehicle (P<0.01). ( E ) Number of rewards earned (Treatment effect: P=0.0078; * P<0.05 vs. vehicle at 5 and 10 mg/kg). ( F ) Water rewards (non-specific control) were unaffected (P=0.57). ( G ) Ethanol intake separated by sex. Two-way ANOVA showed main effects of dose (P=0.0001) and sex (P=0.0011) but no interaction. ( H ) Males only: significant treatment effect (P=0.0073; * P<0.05 at 5 and 10 mg/kg). ( I ) Females only: significant treatment effect (P=0.0279; * P<0.05 at 10 mg/kg). Data expressed as mean ± SEM.

Article Snippet: Ivermectin (MedChemExpress, Monmouth Junction, NJ, USA) was freshly dissolved in a vehicle containing 95% physiological saline (0.9% NaCl) and 5% Tween 80 and administered intraperitoneally (i.p.) 4 hours before behavioral testing, using a Latin Square design.

Techniques: Control

All panels depict data from the cohort (n = 32; 16 males, 16 females) stratified into non-responders (n = 11), mild responders (n = 10), and responders (n = 11) based on averaged Z-scores of deltas decrease in intake across ivermectin doses. ( A ) Averaged responsivity Z-scores by group, with one-way ANOVA showing a significant group effect (P < 0.0001). Bonferroni’s post-hoc tests indicated differences between non-responders and responders (****P < 0.0001) and mild responders and responders (***P = 0.0003). Data are presented as mean ± SEM. ( B ) Correlation between baseline post-vapor ethanol intake Z-scores and responsivity Z-scores (linear regression: R 2 = 0.3334, P = 0.0007). ( C ) Average blood alcohol levels (BALs; mg/dL) during vapor exposure showed no group differences (ANOVA: P = 0.4460). Data are presented as mean ± SEM. ( D ) Ethanol intake (g/kg) across doses in non-responders showed no significant treatment effect (ANOVA: P = 0.0774). Data presented as mean ± SEM. ( E ) Ethanol intake in mild responders exhibited a significant treatment effect (ANOVA: P = 0.0091) and post-hoc tests showing reductions at 5 and 10 mg/kg (*P < 0.05). Data are presented as mean ± SEM. ( F ) Ethanol intake in responders demonstrated a significant treatment effect (ANOVA: P < 0.0001) and post-hoc tests indicating reductions at all doses (*P < 0.05, **P < 0.01, ***P < 0.001). Data are presented as mean ± SEM. In all panels, individual data points are shown as blue dots (males) and pink dots (females).

Journal: Neuropharmacology

Article Title: Ivermectin Reduces Withdrawal-Induced Alcohol Intake in Rats: Association with CeA GABAergic Enhancement and P2rx4 Genetic Liability

doi: 10.1016/j.neuropharm.2026.110881

Figure Lengend Snippet: All panels depict data from the cohort (n = 32; 16 males, 16 females) stratified into non-responders (n = 11), mild responders (n = 10), and responders (n = 11) based on averaged Z-scores of deltas decrease in intake across ivermectin doses. ( A ) Averaged responsivity Z-scores by group, with one-way ANOVA showing a significant group effect (P < 0.0001). Bonferroni’s post-hoc tests indicated differences between non-responders and responders (****P < 0.0001) and mild responders and responders (***P = 0.0003). Data are presented as mean ± SEM. ( B ) Correlation between baseline post-vapor ethanol intake Z-scores and responsivity Z-scores (linear regression: R 2 = 0.3334, P = 0.0007). ( C ) Average blood alcohol levels (BALs; mg/dL) during vapor exposure showed no group differences (ANOVA: P = 0.4460). Data are presented as mean ± SEM. ( D ) Ethanol intake (g/kg) across doses in non-responders showed no significant treatment effect (ANOVA: P = 0.0774). Data presented as mean ± SEM. ( E ) Ethanol intake in mild responders exhibited a significant treatment effect (ANOVA: P = 0.0091) and post-hoc tests showing reductions at 5 and 10 mg/kg (*P < 0.05). Data are presented as mean ± SEM. ( F ) Ethanol intake in responders demonstrated a significant treatment effect (ANOVA: P < 0.0001) and post-hoc tests indicating reductions at all doses (*P < 0.05, **P < 0.01, ***P < 0.001). Data are presented as mean ± SEM. In all panels, individual data points are shown as blue dots (males) and pink dots (females).

Article Snippet: Ivermectin (MedChemExpress, Monmouth Junction, NJ, USA) was freshly dissolved in a vehicle containing 95% physiological saline (0.9% NaCl) and 5% Tween 80 and administered intraperitoneally (i.p.) 4 hours before behavioral testing, using a Latin Square design.

Techniques:

(A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with ivermectin (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Journal: bioRxiv

Article Title: Deep phenotypic profiling uncovers cryptic effects of antifilarial drugs

doi: 10.64898/2026.02.12.705610

Figure Lengend Snippet: (A) Schematic depicting the methodology and time points of mf motility and viability data collection. (B) Motility dose response curves 24 hours and 48 hours after treatment with ivermectin (IVM), diethylcarbamazine (DEC), albendazole sulfoxide (AZS), and emodepside (EMO), with dashed lines showing experimental IC50 (color) and therapeutic plasma C max (black) values. Controls include mf treated with 1% DMSO and heat killed (HK) mf. (C) Viability (CellTox Green) fluorescence readings on a log 10 scale across treatment concentrations compared to DMSO and HK controls. (D) Representative brightfield (top row) and CellTox stained (bottom row) images of control and drug treated mf. (E) Motility dose response curves for drug treatment combinations. IVM treatment combined with AZS (500nM or 10µM) or DEC (15µM or 30µM), and EMO treatment combined with 15µM or 30µM DEC. Drug combination IC50s are marked as solid colored lines and IVM plasma C max values as dashed black lines. Individual drug IC50s from (B) are also shown (IVM: purple, EMO: green). Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least four technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Article Snippet: Compounds were sourced as follows: ivermectin (MP Biomedicals, LLC), diethylcarbamazine (MP Biomedicals, LLC), albendazole sulfoxide (Sigma-Aldrich), emodepside (Advanced ChemBlocks, Inc).

Techniques: Clinical Proteomics, CellTox Assay, Fluorescence, Staining, Control

(A) Schematic showing methodology and timeline for mf temperature shift assay. (B) Mean motility, scaled to DMSO 1 hour values of B. pahangi mf at 37℃ (left panel) and room temperature (RT, right panel) across time and ivermectin (IVM) or control treatment concentrations (color-coded). P-values represent statistical differences in mf motility between DMSO and drug treatments at matched time points and temperature and were calculated using Anova/Tukey post-test and significance reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least six technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Journal: bioRxiv

Article Title: Deep phenotypic profiling uncovers cryptic effects of antifilarial drugs

doi: 10.64898/2026.02.12.705610

Figure Lengend Snippet: (A) Schematic showing methodology and timeline for mf temperature shift assay. (B) Mean motility, scaled to DMSO 1 hour values of B. pahangi mf at 37℃ (left panel) and room temperature (RT, right panel) across time and ivermectin (IVM) or control treatment concentrations (color-coded). P-values represent statistical differences in mf motility between DMSO and drug treatments at matched time points and temperature and were calculated using Anova/Tukey post-test and significance reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least six technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Article Snippet: Compounds were sourced as follows: ivermectin (MP Biomedicals, LLC), diethylcarbamazine (MP Biomedicals, LLC), albendazole sulfoxide (Sigma-Aldrich), emodepside (Advanced ChemBlocks, Inc).

Techniques: Shift Assay, Control

(A) Schematic depicting the salt assay methodology and timeline. (B) Top two bar graph panels indicate combinations of KPO 4 concentrations (10mM, 25mM, 50mM, and 100mM) and NaCl concentrations (25mM, 50mM, 100mM, 125mM, and 150mM) across the remaining figure panels at vertically aligned positions. The bottom panel shows DMSO-treated B. pahangi mf motility in the presence of different concentrations of NaCl and KPO 4 across time points. (C) The top and bottom panels show optical flow differences between DMSO and ivermectin (IVM) treated B. pahangi mf (delta motility) at varying salt combinations in the presence of 50nM (top panel) or 500nM (bottom panel) IVM. P-values representing statistical differences in mf motility between DMSO and IVM treatments were calculated using Anova/Tukey post-test and significance is reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least two technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Journal: bioRxiv

Article Title: Deep phenotypic profiling uncovers cryptic effects of antifilarial drugs

doi: 10.64898/2026.02.12.705610

Figure Lengend Snippet: (A) Schematic depicting the salt assay methodology and timeline. (B) Top two bar graph panels indicate combinations of KPO 4 concentrations (10mM, 25mM, 50mM, and 100mM) and NaCl concentrations (25mM, 50mM, 100mM, 125mM, and 150mM) across the remaining figure panels at vertically aligned positions. The bottom panel shows DMSO-treated B. pahangi mf motility in the presence of different concentrations of NaCl and KPO 4 across time points. (C) The top and bottom panels show optical flow differences between DMSO and ivermectin (IVM) treated B. pahangi mf (delta motility) at varying salt combinations in the presence of 50nM (top panel) or 500nM (bottom panel) IVM. P-values representing statistical differences in mf motility between DMSO and IVM treatments were calculated using Anova/Tukey post-test and significance is reported as follows, * : p<0.05, ** : p<0.01, *** : p<0.001. Each plot point represents measurements for a plate well containing 1000 mf; each condition was performed across at least two technical replicates (wells) per experiment and each experiment was repeated for at least three biological replicates (parasite cohorts).

Article Snippet: Compounds were sourced as follows: ivermectin (MP Biomedicals, LLC), diethylcarbamazine (MP Biomedicals, LLC), albendazole sulfoxide (Sigma-Aldrich), emodepside (Advanced ChemBlocks, Inc).

Techniques: