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sn38  (MedChemExpress)


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    Structured Review

    MedChemExpress sn38
    Sn38, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sn38/product/MedChemExpress
    Average 95 stars, based on 50 article reviews
    sn38 - by Bioz Stars, 2026-02
    95/100 stars

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    MedChemExpress sn38
    Sn38, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MedChemExpress irinotecan
    THM combined with clinical medications exhibited significant synergistic antitumor effect in colorectal cancer animal models. A HCT116 tumor-bearing athymic nude mice tumor inoculation [subcutaneous (s.c.)] and treatment plan. Nine days after tumor inoculation, mice were treated intraperitoneally with THM medium dose, Cetuximab, FOLFOX regimen (5-FU + Calcium levofolinate + Oxaliplatin), FOLFIRI regimen (5-FU + Calcium levofolinate + <t>Irinotecan),</t> THM + Cetuximab, THM + FOLFOX, and THM + FOLFIRI. The THM mid-dose group received 60 mg/kg every other day and the Cetuximab group received 1 mg/mouse daily. FOLFOX group received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Oxaliplatin (9.375 mg/kg) on days 2 and 9. FOLFIRI received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Iirinotecan (15 mg/kg) on days 2 and 9. B Photographs of the excised tumors from HCT116 xenograft bearing mice across different treatment groups were captured on day 20 ( n = 5). C-D The average tumor growth curves of all treatment groups. Data was shown as mean ± SD ( n = 5), and significance was determined using two-way ANOVA with Tukey’s multiple comparisons test (*** p < 0.001 and **** p < 0.0001). E Average body weight of HCT116 tumor-bearing mice during the treatment. Data was shown as mean ± SD ( n = 5). F-H Schematic diagrams for calculating the combination index (CI) after treatment with THM in combination with Cetuximab (F), the FOLFOX regimen (G), and the FOLFIRI regimen (H). Data was shown as mean ± SD ( n = 5), * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by one-way ANOVA with Tukey’s multiple comparisons test. I Immunohistochemical staining of PANoptosis indexes by subcutaneous tumor-bearing HCT116 colorectal cancer tumor tissue sections combined with clinical drugs (Cetuximab, FOLFOX and FOLFIRI regimens)
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    TargetMol irinotecan
    Maritoclax enhanced the antitumor effect of <t>irinotecan</t> on FBW7 R465C‐overexpressed CRC in vivo. HA‐Vec (wild‐type group) or HA‐FBW7 R465C ‐overexpressed (R465C‐mutation group) HCT‐116 cells were subcutaneously injected into 5‐week‐old female BALB/c nude mice. Drugs were administered every 4 days after tumor volume reached 100 mm 3 . Nude mice in the wild‐type group were assigned to vehicle (DMSO) or irinotecan (35 mg/kg) treatment groups and those in R465C‐mutation group were divided into four groups that treated with vehicle (DMSO), irinotecan (35 mg/kg), Maritoclax (5 mg/kg), or irinotecan (35 mg/kg) plus Maritoclax (5 mg/kg), respectively. Nude mice were sacrificed when tumor volume reached 1500 mm 3 or diameter reached 20 mm. (A, D) Tumors were dissected and recorded by photographed. (B, E) Tumor volumes (length*width 2 /2) and (C, F) body weights of mice were recorded every other day during treatment. Western blot was performed to detect the protein level of MCL1 in tumor tissues from (G) the wild‐type and R465C‐mutation control groups; (H) the wild‐type control group and R465C‐mutation groups including control, irinotecan monotherapy, Maritoclax monotherapy, and combination therapy. Data are expressed as the mean ± SD ( n = 3, representing three independent experiments). p values were calculated by using Two‐way ANOVA or Student's t ‐test, the coloration of the p ‐value markers is consistent with the color scheme of each corresponding group. ns: p > 0.05, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the vehicle group; ### p < 0.001, ## p < 0.01, # p < 0.05 vs. the irinotecan group; ++ p < 0.01, + p < 0.05 vs. the Maritoclax group.
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    MedChemExpress sn 38
    Maritoclax enhanced the antitumor effect of <t>irinotecan</t> on FBW7 R465C‐overexpressed CRC in vivo. HA‐Vec (wild‐type group) or HA‐FBW7 R465C ‐overexpressed (R465C‐mutation group) HCT‐116 cells were subcutaneously injected into 5‐week‐old female BALB/c nude mice. Drugs were administered every 4 days after tumor volume reached 100 mm 3 . Nude mice in the wild‐type group were assigned to vehicle (DMSO) or irinotecan (35 mg/kg) treatment groups and those in R465C‐mutation group were divided into four groups that treated with vehicle (DMSO), irinotecan (35 mg/kg), Maritoclax (5 mg/kg), or irinotecan (35 mg/kg) plus Maritoclax (5 mg/kg), respectively. Nude mice were sacrificed when tumor volume reached 1500 mm 3 or diameter reached 20 mm. (A, D) Tumors were dissected and recorded by photographed. (B, E) Tumor volumes (length*width 2 /2) and (C, F) body weights of mice were recorded every other day during treatment. Western blot was performed to detect the protein level of MCL1 in tumor tissues from (G) the wild‐type and R465C‐mutation control groups; (H) the wild‐type control group and R465C‐mutation groups including control, irinotecan monotherapy, Maritoclax monotherapy, and combination therapy. Data are expressed as the mean ± SD ( n = 3, representing three independent experiments). p values were calculated by using Two‐way ANOVA or Student's t ‐test, the coloration of the p ‐value markers is consistent with the color scheme of each corresponding group. ns: p > 0.05, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the vehicle group; ### p < 0.001, ## p < 0.01, # p < 0.05 vs. the irinotecan group; ++ p < 0.01, + p < 0.05 vs. the Maritoclax group.
    Sn 38, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    THM combined with clinical medications exhibited significant synergistic antitumor effect in colorectal cancer animal models. A HCT116 tumor-bearing athymic nude mice tumor inoculation [subcutaneous (s.c.)] and treatment plan. Nine days after tumor inoculation, mice were treated intraperitoneally with THM medium dose, Cetuximab, FOLFOX regimen (5-FU + Calcium levofolinate + Oxaliplatin), FOLFIRI regimen (5-FU + Calcium levofolinate + Irinotecan), THM + Cetuximab, THM + FOLFOX, and THM + FOLFIRI. The THM mid-dose group received 60 mg/kg every other day and the Cetuximab group received 1 mg/mouse daily. FOLFOX group received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Oxaliplatin (9.375 mg/kg) on days 2 and 9. FOLFIRI received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Iirinotecan (15 mg/kg) on days 2 and 9. B Photographs of the excised tumors from HCT116 xenograft bearing mice across different treatment groups were captured on day 20 ( n = 5). C-D The average tumor growth curves of all treatment groups. Data was shown as mean ± SD ( n = 5), and significance was determined using two-way ANOVA with Tukey’s multiple comparisons test (*** p < 0.001 and **** p < 0.0001). E Average body weight of HCT116 tumor-bearing mice during the treatment. Data was shown as mean ± SD ( n = 5). F-H Schematic diagrams for calculating the combination index (CI) after treatment with THM in combination with Cetuximab (F), the FOLFOX regimen (G), and the FOLFIRI regimen (H). Data was shown as mean ± SD ( n = 5), * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by one-way ANOVA with Tukey’s multiple comparisons test. I Immunohistochemical staining of PANoptosis indexes by subcutaneous tumor-bearing HCT116 colorectal cancer tumor tissue sections combined with clinical drugs (Cetuximab, FOLFOX and FOLFIRI regimens)

    Journal: Experimental Hematology & Oncology

    Article Title: Tetrahydromagnolol targets TRIM38 to mediate PANoptosis in cancer cells and has the potential for synergistic cancer therapy

    doi: 10.1186/s40164-025-00734-4

    Figure Lengend Snippet: THM combined with clinical medications exhibited significant synergistic antitumor effect in colorectal cancer animal models. A HCT116 tumor-bearing athymic nude mice tumor inoculation [subcutaneous (s.c.)] and treatment plan. Nine days after tumor inoculation, mice were treated intraperitoneally with THM medium dose, Cetuximab, FOLFOX regimen (5-FU + Calcium levofolinate + Oxaliplatin), FOLFIRI regimen (5-FU + Calcium levofolinate + Irinotecan), THM + Cetuximab, THM + FOLFOX, and THM + FOLFIRI. The THM mid-dose group received 60 mg/kg every other day and the Cetuximab group received 1 mg/mouse daily. FOLFOX group received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Oxaliplatin (9.375 mg/kg) on days 2 and 9. FOLFIRI received 5-FU (22.5 mg/kg) and Calcium levofolinate (33.75 mg/kg) on days 1 and 8 and Iirinotecan (15 mg/kg) on days 2 and 9. B Photographs of the excised tumors from HCT116 xenograft bearing mice across different treatment groups were captured on day 20 ( n = 5). C-D The average tumor growth curves of all treatment groups. Data was shown as mean ± SD ( n = 5), and significance was determined using two-way ANOVA with Tukey’s multiple comparisons test (*** p < 0.001 and **** p < 0.0001). E Average body weight of HCT116 tumor-bearing mice during the treatment. Data was shown as mean ± SD ( n = 5). F-H Schematic diagrams for calculating the combination index (CI) after treatment with THM in combination with Cetuximab (F), the FOLFOX regimen (G), and the FOLFIRI regimen (H). Data was shown as mean ± SD ( n = 5), * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 by one-way ANOVA with Tukey’s multiple comparisons test. I Immunohistochemical staining of PANoptosis indexes by subcutaneous tumor-bearing HCT116 colorectal cancer tumor tissue sections combined with clinical drugs (Cetuximab, FOLFOX and FOLFIRI regimens)

    Article Snippet: 5-Fluorouracil (5-FU) (HY-9006), Irinotecan (HY-16562), Calcium levofolinate (HY-13667), Oxaliplatin (HY-17371), Necrostatin-1 (Nec-1) (HY-15760), Z-VAD-FMK (HY-16658B), Ferrostatin-1 (Fer-1) (HY-100579), Chloroquine (CQ) (HY-175889A) were acquired from MCE (Monmouth Junction, NJ, USA).

    Techniques: Medications, Immunohistochemical staining, Staining

    Maritoclax enhanced the antitumor effect of irinotecan on FBW7 R465C‐overexpressed CRC in vivo. HA‐Vec (wild‐type group) or HA‐FBW7 R465C ‐overexpressed (R465C‐mutation group) HCT‐116 cells were subcutaneously injected into 5‐week‐old female BALB/c nude mice. Drugs were administered every 4 days after tumor volume reached 100 mm 3 . Nude mice in the wild‐type group were assigned to vehicle (DMSO) or irinotecan (35 mg/kg) treatment groups and those in R465C‐mutation group were divided into four groups that treated with vehicle (DMSO), irinotecan (35 mg/kg), Maritoclax (5 mg/kg), or irinotecan (35 mg/kg) plus Maritoclax (5 mg/kg), respectively. Nude mice were sacrificed when tumor volume reached 1500 mm 3 or diameter reached 20 mm. (A, D) Tumors were dissected and recorded by photographed. (B, E) Tumor volumes (length*width 2 /2) and (C, F) body weights of mice were recorded every other day during treatment. Western blot was performed to detect the protein level of MCL1 in tumor tissues from (G) the wild‐type and R465C‐mutation control groups; (H) the wild‐type control group and R465C‐mutation groups including control, irinotecan monotherapy, Maritoclax monotherapy, and combination therapy. Data are expressed as the mean ± SD ( n = 3, representing three independent experiments). p values were calculated by using Two‐way ANOVA or Student's t ‐test, the coloration of the p ‐value markers is consistent with the color scheme of each corresponding group. ns: p > 0.05, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the vehicle group; ### p < 0.001, ## p < 0.01, # p < 0.05 vs. the irinotecan group; ++ p < 0.01, + p < 0.05 vs. the Maritoclax group.

    Journal: Cancer Medicine

    Article Title: Maritoclax Overcomes FBW7 Deficiency‐Driven Irinotecan Resistance in Colorectal Cancer by Targeting MCL1

    doi: 10.1002/cam4.71419

    Figure Lengend Snippet: Maritoclax enhanced the antitumor effect of irinotecan on FBW7 R465C‐overexpressed CRC in vivo. HA‐Vec (wild‐type group) or HA‐FBW7 R465C ‐overexpressed (R465C‐mutation group) HCT‐116 cells were subcutaneously injected into 5‐week‐old female BALB/c nude mice. Drugs were administered every 4 days after tumor volume reached 100 mm 3 . Nude mice in the wild‐type group were assigned to vehicle (DMSO) or irinotecan (35 mg/kg) treatment groups and those in R465C‐mutation group were divided into four groups that treated with vehicle (DMSO), irinotecan (35 mg/kg), Maritoclax (5 mg/kg), or irinotecan (35 mg/kg) plus Maritoclax (5 mg/kg), respectively. Nude mice were sacrificed when tumor volume reached 1500 mm 3 or diameter reached 20 mm. (A, D) Tumors were dissected and recorded by photographed. (B, E) Tumor volumes (length*width 2 /2) and (C, F) body weights of mice were recorded every other day during treatment. Western blot was performed to detect the protein level of MCL1 in tumor tissues from (G) the wild‐type and R465C‐mutation control groups; (H) the wild‐type control group and R465C‐mutation groups including control, irinotecan monotherapy, Maritoclax monotherapy, and combination therapy. Data are expressed as the mean ± SD ( n = 3, representing three independent experiments). p values were calculated by using Two‐way ANOVA or Student's t ‐test, the coloration of the p ‐value markers is consistent with the color scheme of each corresponding group. ns: p > 0.05, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05 vs. the vehicle group; ### p < 0.001, ## p < 0.01, # p < 0.05 vs. the irinotecan group; ++ p < 0.01, + p < 0.05 vs. the Maritoclax group.

    Article Snippet: Irinotecan (Cat# T6228; Targetmol), SN38 (Cat# T1703; Targetmol), Marinopyrrole A (Maritoclax, Cat# T11944 ; Targetmol) and MG132 (Cat# MB5137‐1; Meilunbio) were dissolved in dimethylsulfoxide (DMSO); puromycin (Cat# MB2005; Meilunbio) was dissolved in sterile deionized water.

    Techniques: In Vivo, Mutagenesis, Injection, Western Blot, Control