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Merck & Co crixivan
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Merck & Co crixivan (indinavir
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Bristol Myers crixivan
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Merck KGaA indinavir (crixivan)
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TargetMol indinavir
Potential inhibitors of SARS-CoV-2 3CL pro selected from approved or commercially available drugs.
Indinavir, supplied by TargetMol, 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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Merck & Co indinavir for in vitro experiments
Rat islets were incubated for 48 hours in the presence and absence of <t>indinavir</t> (20 μM) at basal (5 mM) and hyperglycemic (22 mM) concentrations of glucose. (A, B) Islets incubated in the absence of indinavir (dark bars) and when carbachol was added to the incubation media. Islets treated with indinavir (light bars) secreted insulin and C-peptide in amounts that were not significantly different from amounts secreted by control islets when glucose concentrations were 5 and 22 mM. (C) Rat islet iPLA2 activity was not suppressed in [beta]-cells treated with indinavir when compared with iPLA2 activity in control [beta]-cells incubated in the absence of indinavir.
Indinavir For In Vitro Experiments, supplied by Merck & Co, 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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Merck & Co indinavir
Evolution of CD4-cell count (number of cells per microliter), viral load (log10 number of copies of RNA per milliliter) and resistance-related genotype of the RT gene for patients SW3 (A) and CHG (B) who harbored viruses with the T69S-SS mutation. The times of retrieval of the original samples included in the screening, SW3-10125 and CHG-4815, respectively, are indicated by the bold arrow. Patient CHG had been treated with zidovudine (ZDV) since December 1990. ddI, didanosine; 3TC, lamivudine; d4T, stavudine; IDV, <t>indinavir;</t> WT, wild type.
Indinavir, supplied by Merck & Co, 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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Thermo Fisher indinavir
Increased glucose uptake through GLUT4 is required to induce cardiomyocyte hypertrophy by testosterone. a Glucose uptake was measured as 2-NBDG uptake (300 µM) and was normalized to the basal level after exposure to 100 nM testosterone for 24 h. Testosterone-induced 2-NBDG uptake was measured in the presence or absence of <t>indinavir.</t> Cardiomyocytes were pretreated with 100 µM indinavir and stimulated with 100 nM testosterone by 24 h. b Cellular area was assessed using the fluorescent dye Rhodamine/Phalloidin, and > 100 cells were analyzed in each condition. c Cardiomyocytes were stimulated with 100 nM testosterone for 10 h and β-mhc mRNA level was determined by RT-qPCR. The mRNA levels were normalized to 18S mRNA levels (n = 6). Data are expressed as mean ± SEM of at least three independent experiments. *P < 0.05, ***P < 0.001 vs. control; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. testosterone
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Millipore indinavir
ATPγS has insulin-mimetic roles in C2C12 myotubes activating PI3K/PKB and mTOR pathway signaling proteins in a P2-receptor-dependent manner and enhancing GLUT4-mediated glucose uptake. (A,B) Representative immunoblots for PKB (pS473) normalized to PKB (A; n = 5) and p70-S6K1 (pT389) normalized to p70-S6K1 (B; n = 6) with densitometric analysis below for cells treated with ATPγS (50–100 μM; 15 min). (Ci) Representative immunoblots for PKB (pS473), PKB, p70-S6K1 (pT389), p70-S6K1, ERK 1/2 (pT202/TY204) and actin for cells treated with ATPγS (50 μM; 15 min) with and without broad spectrum P2 receptor antagonists PPADs (100 μM) and suramin (100 μM), P2X4R antagonist 5-BDBD (5 μM) and P2X7R antagonist A438079 (100 μM) (45 min prior to spiked ATPγS; n = 6). Densitometric analysis for p70-S6K1 (pT389) normalized to p70-S6K1 in (Cii) ; PKB (pS473) normalized to PKB in (Ciii) and ERK 1/2 (pT202/TY204) normalized to actin in (Civ) . (D) Glucose uptake (2-DG; 100 μM; 15 min) assessed by luminescence following treatment with ATPγS (0–100 μM; 15 min pre-treatment) or insulin (200 nM; 15 min pre-treatment) ( n = 9). (E) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with ATPγS (100 μM; 15 min) in the presence or absence of GLUT4 inhibitor <t>indinavir</t> (50 μM) ( n = 5). (F) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with palmitate (500 μM; 16 h) and ATPγS (100 μM; 15 min) ( n = 17). * P < 0.05; ** P < 0.01; *** P < 0.001 against untreated control, $$$ P < 0.001 against ATPγS control.
Indinavir, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fisher Scientific indinavir
ATPγS has insulin-mimetic roles in C2C12 myotubes activating PI3K/PKB and mTOR pathway signaling proteins in a P2-receptor-dependent manner and enhancing GLUT4-mediated glucose uptake. (A,B) Representative immunoblots for PKB (pS473) normalized to PKB (A; n = 5) and p70-S6K1 (pT389) normalized to p70-S6K1 (B; n = 6) with densitometric analysis below for cells treated with ATPγS (50–100 μM; 15 min). (Ci) Representative immunoblots for PKB (pS473), PKB, p70-S6K1 (pT389), p70-S6K1, ERK 1/2 (pT202/TY204) and actin for cells treated with ATPγS (50 μM; 15 min) with and without broad spectrum P2 receptor antagonists PPADs (100 μM) and suramin (100 μM), P2X4R antagonist 5-BDBD (5 μM) and P2X7R antagonist A438079 (100 μM) (45 min prior to spiked ATPγS; n = 6). Densitometric analysis for p70-S6K1 (pT389) normalized to p70-S6K1 in (Cii) ; PKB (pS473) normalized to PKB in (Ciii) and ERK 1/2 (pT202/TY204) normalized to actin in (Civ) . (D) Glucose uptake (2-DG; 100 μM; 15 min) assessed by luminescence following treatment with ATPγS (0–100 μM; 15 min pre-treatment) or insulin (200 nM; 15 min pre-treatment) ( n = 9). (E) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with ATPγS (100 μM; 15 min) in the presence or absence of GLUT4 inhibitor <t>indinavir</t> (50 μM) ( n = 5). (F) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with palmitate (500 μM; 16 h) and ATPγS (100 μM; 15 min) ( n = 17). * P < 0.05; ** P < 0.01; *** P < 0.001 against untreated control, $$$ P < 0.001 against ATPγS control.
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Stada Arzneimittel indinavir
Characteristics of 231 patients on second-line ART in HCMC
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Videx Inc epivir 3tc/lamivudine
Characteristics of 231 patients on second-line ART in HCMC
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Image Search Results


Potential inhibitors of SARS-CoV-2 3CL pro selected from approved or commercially available drugs.

Journal: Computational and Structural Biotechnology Journal

Article Title: An overview of potential inhibitors targeting non-structural proteins 3 (PL pro and Mac1) and 5 (3CL pro /M pro ) of SARS-CoV-2

doi: 10.1016/j.csbj.2021.08.036

Figure Lengend Snippet: Potential inhibitors of SARS-CoV-2 3CL pro selected from approved or commercially available drugs.

Article Snippet: Selleckchem; Targetmol , , 3,118 FDA-approved drugs , Angiotensin II; GHRP-2; Indinavir; Polymyxin B; Fexofenadine; Atazanavir ; Cobicistat; Caspofungin; Lopinavir.

Techniques:

Potential inhibitors of SARS-CoV-2 3CL pro selected from existing databases or literature.

Journal: Computational and Structural Biotechnology Journal

Article Title: An overview of potential inhibitors targeting non-structural proteins 3 (PL pro and Mac1) and 5 (3CL pro /M pro ) of SARS-CoV-2

doi: 10.1016/j.csbj.2021.08.036

Figure Lengend Snippet: Potential inhibitors of SARS-CoV-2 3CL pro selected from existing databases or literature.

Article Snippet: Selleckchem; Targetmol , , 3,118 FDA-approved drugs , Angiotensin II; GHRP-2; Indinavir; Polymyxin B; Fexofenadine; Atazanavir ; Cobicistat; Caspofungin; Lopinavir.

Techniques:

Rat islets were incubated for 48 hours in the presence and absence of indinavir (20 μM) at basal (5 mM) and hyperglycemic (22 mM) concentrations of glucose. (A, B) Islets incubated in the absence of indinavir (dark bars) and when carbachol was added to the incubation media. Islets treated with indinavir (light bars) secreted insulin and C-peptide in amounts that were not significantly different from amounts secreted by control islets when glucose concentrations were 5 and 22 mM. (C) Rat islet iPLA2 activity was not suppressed in [beta]-cells treated with indinavir when compared with iPLA2 activity in control [beta]-cells incubated in the absence of indinavir.

Journal: Journal of acquired immune deficiency syndromes (1999)

Article Title: Insulin Resistance in HIV Protease Inhibitor-Associated Diabetes

doi:

Figure Lengend Snippet: Rat islets were incubated for 48 hours in the presence and absence of indinavir (20 μM) at basal (5 mM) and hyperglycemic (22 mM) concentrations of glucose. (A, B) Islets incubated in the absence of indinavir (dark bars) and when carbachol was added to the incubation media. Islets treated with indinavir (light bars) secreted insulin and C-peptide in amounts that were not significantly different from amounts secreted by control islets when glucose concentrations were 5 and 22 mM. (C) Rat islet iPLA2 activity was not suppressed in [beta]-cells treated with indinavir when compared with iPLA2 activity in control [beta]-cells incubated in the absence of indinavir.

Article Snippet: Indinavir for in vitro experiments was obtained from Merck Research Laboratories.

Techniques: Incubation, Activity Assay

Evolution of CD4-cell count (number of cells per microliter), viral load (log10 number of copies of RNA per milliliter) and resistance-related genotype of the RT gene for patients SW3 (A) and CHG (B) who harbored viruses with the T69S-SS mutation. The times of retrieval of the original samples included in the screening, SW3-10125 and CHG-4815, respectively, are indicated by the bold arrow. Patient CHG had been treated with zidovudine (ZDV) since December 1990. ddI, didanosine; 3TC, lamivudine; d4T, stavudine; IDV, indinavir; WT, wild type.

Journal:

Article Title: Prevalence and Characteristics of Multinucleoside-Resistant Human Immunodeficiency Virus Type 1 among European Patients Receiving Combinations of Nucleoside Analogues

doi:

Figure Lengend Snippet: Evolution of CD4-cell count (number of cells per microliter), viral load (log10 number of copies of RNA per milliliter) and resistance-related genotype of the RT gene for patients SW3 (A) and CHG (B) who harbored viruses with the T69S-SS mutation. The times of retrieval of the original samples included in the screening, SW3-10125 and CHG-4815, respectively, are indicated by the bold arrow. Patient CHG had been treated with zidovudine (ZDV) since December 1990. ddI, didanosine; 3TC, lamivudine; d4T, stavudine; IDV, indinavir; WT, wild type.

Article Snippet: ; indinavir was purchased from Merck Research Laboratories, West Point, Pa.; saquinavir was purchased from Roche Products Limited, Welwyn Garden City, United Kingdom; ritonavir was purchased from Abbott Laboratories, Abbott Park, Ill.; and nelfinavir was purchased from Agouron Pharmaceuticals, La Jolla, Calif. EC 50 s were compared to the mean EC 50 s for a control wild-type strain (HIV-1 III B ) and were expressed as fold resistance.

Techniques: Cell Counting, Mutagenesis

Increased glucose uptake through GLUT4 is required to induce cardiomyocyte hypertrophy by testosterone. a Glucose uptake was measured as 2-NBDG uptake (300 µM) and was normalized to the basal level after exposure to 100 nM testosterone for 24 h. Testosterone-induced 2-NBDG uptake was measured in the presence or absence of indinavir. Cardiomyocytes were pretreated with 100 µM indinavir and stimulated with 100 nM testosterone by 24 h. b Cellular area was assessed using the fluorescent dye Rhodamine/Phalloidin, and > 100 cells were analyzed in each condition. c Cardiomyocytes were stimulated with 100 nM testosterone for 10 h and β-mhc mRNA level was determined by RT-qPCR. The mRNA levels were normalized to 18S mRNA levels (n = 6). Data are expressed as mean ± SEM of at least three independent experiments. *P < 0.05, ***P < 0.001 vs. control; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. testosterone

Journal: Biological Research

Article Title: Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy

doi: 10.1186/s40659-021-00328-4

Figure Lengend Snippet: Increased glucose uptake through GLUT4 is required to induce cardiomyocyte hypertrophy by testosterone. a Glucose uptake was measured as 2-NBDG uptake (300 µM) and was normalized to the basal level after exposure to 100 nM testosterone for 24 h. Testosterone-induced 2-NBDG uptake was measured in the presence or absence of indinavir. Cardiomyocytes were pretreated with 100 µM indinavir and stimulated with 100 nM testosterone by 24 h. b Cellular area was assessed using the fluorescent dye Rhodamine/Phalloidin, and > 100 cells were analyzed in each condition. c Cardiomyocytes were stimulated with 100 nM testosterone for 10 h and β-mhc mRNA level was determined by RT-qPCR. The mRNA levels were normalized to 18S mRNA levels (n = 6). Data are expressed as mean ± SEM of at least three independent experiments. *P < 0.05, ***P < 0.001 vs. control; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. testosterone

Article Snippet: Testosterone, 5-bromo-2-deoxyuridine (BrdU), compound C (CC), bicalutamide, indinavir, insulin, 2-NBDG [2-(N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2-deoxyglucose], Rhodamine/Phalloidin, RIPA and Dako mounting medium were from Thermo-Fisher Scientific (Rockford, IL, USA).

Techniques: Quantitative RT-PCR

ATPγS has insulin-mimetic roles in C2C12 myotubes activating PI3K/PKB and mTOR pathway signaling proteins in a P2-receptor-dependent manner and enhancing GLUT4-mediated glucose uptake. (A,B) Representative immunoblots for PKB (pS473) normalized to PKB (A; n = 5) and p70-S6K1 (pT389) normalized to p70-S6K1 (B; n = 6) with densitometric analysis below for cells treated with ATPγS (50–100 μM; 15 min). (Ci) Representative immunoblots for PKB (pS473), PKB, p70-S6K1 (pT389), p70-S6K1, ERK 1/2 (pT202/TY204) and actin for cells treated with ATPγS (50 μM; 15 min) with and without broad spectrum P2 receptor antagonists PPADs (100 μM) and suramin (100 μM), P2X4R antagonist 5-BDBD (5 μM) and P2X7R antagonist A438079 (100 μM) (45 min prior to spiked ATPγS; n = 6). Densitometric analysis for p70-S6K1 (pT389) normalized to p70-S6K1 in (Cii) ; PKB (pS473) normalized to PKB in (Ciii) and ERK 1/2 (pT202/TY204) normalized to actin in (Civ) . (D) Glucose uptake (2-DG; 100 μM; 15 min) assessed by luminescence following treatment with ATPγS (0–100 μM; 15 min pre-treatment) or insulin (200 nM; 15 min pre-treatment) ( n = 9). (E) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with ATPγS (100 μM; 15 min) in the presence or absence of GLUT4 inhibitor indinavir (50 μM) ( n = 5). (F) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with palmitate (500 μM; 16 h) and ATPγS (100 μM; 15 min) ( n = 17). * P < 0.05; ** P < 0.01; *** P < 0.001 against untreated control, $$$ P < 0.001 against ATPγS control.

Journal: Frontiers in Physiology

Article Title: Extracellular ATP Increases Glucose Metabolism in Skeletal Muscle Cells in a P2 Receptor Dependent Manner but Does Not Contribute to Palmitate-Induced Insulin Resistance

doi: 10.3389/fphys.2020.567378

Figure Lengend Snippet: ATPγS has insulin-mimetic roles in C2C12 myotubes activating PI3K/PKB and mTOR pathway signaling proteins in a P2-receptor-dependent manner and enhancing GLUT4-mediated glucose uptake. (A,B) Representative immunoblots for PKB (pS473) normalized to PKB (A; n = 5) and p70-S6K1 (pT389) normalized to p70-S6K1 (B; n = 6) with densitometric analysis below for cells treated with ATPγS (50–100 μM; 15 min). (Ci) Representative immunoblots for PKB (pS473), PKB, p70-S6K1 (pT389), p70-S6K1, ERK 1/2 (pT202/TY204) and actin for cells treated with ATPγS (50 μM; 15 min) with and without broad spectrum P2 receptor antagonists PPADs (100 μM) and suramin (100 μM), P2X4R antagonist 5-BDBD (5 μM) and P2X7R antagonist A438079 (100 μM) (45 min prior to spiked ATPγS; n = 6). Densitometric analysis for p70-S6K1 (pT389) normalized to p70-S6K1 in (Cii) ; PKB (pS473) normalized to PKB in (Ciii) and ERK 1/2 (pT202/TY204) normalized to actin in (Civ) . (D) Glucose uptake (2-DG; 100 μM; 15 min) assessed by luminescence following treatment with ATPγS (0–100 μM; 15 min pre-treatment) or insulin (200 nM; 15 min pre-treatment) ( n = 9). (E) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with ATPγS (100 μM; 15 min) in the presence or absence of GLUT4 inhibitor indinavir (50 μM) ( n = 5). (F) Glucose uptake (2-DG; 100 μM; 15 min) following treatment with palmitate (500 μM; 16 h) and ATPγS (100 μM; 15 min) ( n = 17). * P < 0.05; ** P < 0.01; *** P < 0.001 against untreated control, $$$ P < 0.001 against ATPγS control.

Article Snippet: ATP (adenosine 5’-triphosphate magnesium salt), apyrase, fatty acid-free BSA, palmitic acid and indinavir were purchased from Sigma Aldrich (Poole, United Kingdom).

Techniques: Western Blot

Characteristics of 231 patients on second-line ART in HCMC

Journal: Journal of Antimicrobial Chemotherapy

Article Title: High prevalence of PI resistance in patients failing second-line ART in Vietnam

doi: 10.1093/jac/dkv385

Figure Lengend Snippet: Characteristics of 231 patients on second-line ART in HCMC

Article Snippet: Indinavir was generically and locally produced (STADA, Vietnam) during this time and was prescribed (without ritonavir boosting) in public and private settings for patients with treatment failure or intolerance on nevirapine before efavirenz became available in 2004.

Techniques: Concentration Assay

Predicted antiretroviral susceptibility among 22 patients experiencing VF on second-line ART in HCMC using the Stanford algorithm. AZT, zidovudine; d4T, stavudine; 3TC, lamivudine; FTC, emtricitabine; ABC, abacavir; ddI, didanosine; TDF, tenofovir disoproxil fumarate; EFV, efavirenz; NVP, nevirapine; ETR, etravirine; RPV, rilpivirine; LPV, lopinavir; IDV, indinavir; NFV, nelfinavir; ATV, atazanavir; FPV, fosamprenavir; SQV, saquinavir; TPV, tipranavir; DRV, darunavir; r, ritonavir-boosted.

Journal: Journal of Antimicrobial Chemotherapy

Article Title: High prevalence of PI resistance in patients failing second-line ART in Vietnam

doi: 10.1093/jac/dkv385

Figure Lengend Snippet: Predicted antiretroviral susceptibility among 22 patients experiencing VF on second-line ART in HCMC using the Stanford algorithm. AZT, zidovudine; d4T, stavudine; 3TC, lamivudine; FTC, emtricitabine; ABC, abacavir; ddI, didanosine; TDF, tenofovir disoproxil fumarate; EFV, efavirenz; NVP, nevirapine; ETR, etravirine; RPV, rilpivirine; LPV, lopinavir; IDV, indinavir; NFV, nelfinavir; ATV, atazanavir; FPV, fosamprenavir; SQV, saquinavir; TPV, tipranavir; DRV, darunavir; r, ritonavir-boosted.

Article Snippet: Indinavir was generically and locally produced (STADA, Vietnam) during this time and was prescribed (without ritonavir boosting) in public and private settings for patients with treatment failure or intolerance on nevirapine before efavirenz became available in 2004.

Techniques:

Factors associated with VF in 231 patients on second-line ART in HCMC

Journal: Journal of Antimicrobial Chemotherapy

Article Title: High prevalence of PI resistance in patients failing second-line ART in Vietnam

doi: 10.1093/jac/dkv385

Figure Lengend Snippet: Factors associated with VF in 231 patients on second-line ART in HCMC

Article Snippet: Indinavir was generically and locally produced (STADA, Vietnam) during this time and was prescribed (without ritonavir boosting) in public and private settings for patients with treatment failure or intolerance on nevirapine before efavirenz became available in 2004.

Techniques: Concentration Assay