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rhlcat medi6012  (MedImmune llc)

 
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    MedImmune llc rhlcat medi6012
    Rhlcat Medi6012, supplied by MedImmune llc, 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/rhlcat+medi6012/rhlcat+medi6012/pmc08525913-81-10-0
    Average 90 stars, based on 1 article reviews
    rhlcat medi6012 - by Bioz Stars, 2026-11
    90/100 stars

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    Related Articles

    Clinical Proteomics:

    Article Title: Plasma lipoprotein-X quantification on filipin-stained gels: monitoring recombinant LCAT treatment ex vivo
    Article Snippet: Precision studies for LP-X in FLD patient plasma are described in supplemental Fig. S2. rhLCAT (MEDI6012) was produced as described before ( 21 ) and was kindly provided by MedImmune.

    Article Title: Plasma lipoprotein-X quantification on filipin-stained gels: monitoring recombinant LCAT treatment ex vivo
    Article Snippet: Precision studies for LP-X in FLD patient plasma are described in Supplemental Figure S2. rhLCAT (MEDI6012) was produced as described before (21) and was kindly provided by Medimmune.

    Article Title: NOVEL LCAT-BASED THERAPEUTIC APPROACHES
    Article Snippet: MedImmune developed a newer and more potent formulation of rhLCAT, MEDI6012, which was also found to raise HDL-C in stable atherosclerosis patients for at least a week after a single infusion.

    Produced:

    Article Title: Plasma lipoprotein-X quantification on filipin-stained gels: monitoring recombinant LCAT treatment ex vivo
    Article Snippet: Precision studies for LP-X in FLD patient plasma are described in supplemental Fig. S2. rhLCAT (MEDI6012) was produced as described before ( 21 ) and was kindly provided by MedImmune.

    Article Title: Plasma lipoprotein-X quantification on filipin-stained gels: monitoring recombinant LCAT treatment ex vivo
    Article Snippet: Precision studies for LP-X in FLD patient plasma are described in Supplemental Figure S2. rhLCAT (MEDI6012) was produced as described before (21) and was kindly provided by Medimmune.

    Article Title: NOVEL LCAT-BASED THERAPEUTIC APPROACHES
    Article Snippet: MedImmune developed a newer and more potent formulation of rhLCAT, MEDI6012, which was also found to raise HDL-C in stable atherosclerosis patients for at least a week after a single infusion.



    Similar Products

    rhlcat medi6012  (MedImmune llc)
    90
    MedImmune llc rhlcat medi6012
    Rhlcat Medi6012, supplied by MedImmune llc, 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/rhlcat+medi6012/rhlcat+medi6012/pmc08525913-81-10-0
    Average 90 stars, based on 1 article reviews
    rhlcat medi6012 - by Bioz Stars, 2026-11
    90/100 stars
    		  Buy from Supplier
    recombinant human lcat (rhlcat) (medi6012)  (MedImmune llc)
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    MedImmune llc recombinant human lcat (rhlcat) (medi6012)
    In vivo treatment with <t>rhLCAT</t> reduces Lp‐X in ANIT‐induced cholestasis. WT mouse plasma electrophoresis at baseline (A), on day 3 after ANIT gavage and on day 3 after ANIT gavage with multiple in vivo injections of rhLCAT (B). Plasma of six WT mice (n = 6) is shown in (A). Following electrophoresis gels were staining with Filipin (top panels) or Sudan Black (bottom panels) as described in Figure . (A) lanes 1, 2 reflect the migration of purified human LDL and VLDL, respectively; lanes 3‐8, WT mouse plasma of distinctive mice. (B) lanes 1‐3 reflect the migration of purified human LDL, VLDL, and HDL respectively, lanes 4‐6 reflect plasma from three individual WT mice plasma on day 3 after ANIT gavage; lanes 7‐9 show the remodeling effect produced by treatment with rhLCAT, in vivo , on mouse plasma, on day 3 after ANIT gavage. Lp‐X is visible by Filipin and, Sudan staining (mouse m3), in lanes 4‐6 below the red (origin, point of application) line. LDL, VLDL, and HDL migrate toward the anode (+, top) and Lp‐X migrates toward the cathode (−, bottom)
    Recombinant Human Lcat (Rhlcat) (Medi6012), supplied by MedImmune llc, 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/rhlcat+medi6012/rhlcat+medi6012/pmc06935572-39-0-8
    Average 90 stars, based on 1 article reviews
    recombinant human lcat (rhlcat) (medi6012) - by Bioz Stars, 2026-11
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    Image Search Results


    In vivo treatment with rhLCAT reduces Lp‐X in ANIT‐induced cholestasis. WT mouse plasma electrophoresis at baseline (A), on day 3 after ANIT gavage and on day 3 after ANIT gavage with multiple in vivo injections of rhLCAT (B). Plasma of six WT mice (n = 6) is shown in (A). Following electrophoresis gels were staining with Filipin (top panels) or Sudan Black (bottom panels) as described in Figure . (A) lanes 1, 2 reflect the migration of purified human LDL and VLDL, respectively; lanes 3‐8, WT mouse plasma of distinctive mice. (B) lanes 1‐3 reflect the migration of purified human LDL, VLDL, and HDL respectively, lanes 4‐6 reflect plasma from three individual WT mice plasma on day 3 after ANIT gavage; lanes 7‐9 show the remodeling effect produced by treatment with rhLCAT, in vivo , on mouse plasma, on day 3 after ANIT gavage. Lp‐X is visible by Filipin and, Sudan staining (mouse m3), in lanes 4‐6 below the red (origin, point of application) line. LDL, VLDL, and HDL migrate toward the anode (+, top) and Lp‐X migrates toward the cathode (−, bottom)

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: In vivo treatment with rhLCAT reduces Lp‐X in ANIT‐induced cholestasis. WT mouse plasma electrophoresis at baseline (A), on day 3 after ANIT gavage and on day 3 after ANIT gavage with multiple in vivo injections of rhLCAT (B). Plasma of six WT mice (n = 6) is shown in (A). Following electrophoresis gels were staining with Filipin (top panels) or Sudan Black (bottom panels) as described in Figure . (A) lanes 1, 2 reflect the migration of purified human LDL and VLDL, respectively; lanes 3‐8, WT mouse plasma of distinctive mice. (B) lanes 1‐3 reflect the migration of purified human LDL, VLDL, and HDL respectively, lanes 4‐6 reflect plasma from three individual WT mice plasma on day 3 after ANIT gavage; lanes 7‐9 show the remodeling effect produced by treatment with rhLCAT, in vivo , on mouse plasma, on day 3 after ANIT gavage. Lp‐X is visible by Filipin and, Sudan staining (mouse m3), in lanes 4‐6 below the red (origin, point of application) line. LDL, VLDL, and HDL migrate toward the anode (+, top) and Lp‐X migrates toward the cathode (−, bottom)

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: In Vivo, Clinical Proteomics, Electrophoresis, Staining, Migration, Purification, Produced

    Baseline lipid levels and LCAT activity

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Baseline lipid levels and LCAT activity

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Activity Assay

    Changes in hepatic function following treatment with ANIT. Mice (WT, LCAT‐Tg, and LCAT‐KO, males, n = 5 per group) were fasted for 4‐6 hours and then bled by retro‐orbital sinus blood collection (~75‐100 μL). Mice were bled before, 1, 2, 3, and 4 days after ANIT gavage via the retro‐orbital sinus. Hepatic function markers, Total Bilirubin (A), Direct Bilirubin (B), Indirect Bilirubin (C), ALT (D), AST (E), and alkaline phosphatase (F.) were measured as described in the section. * P <.05 compared to WT and LCAT‐Tg mice, # P <.05 compared to LCAT‐Tg mice

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Changes in hepatic function following treatment with ANIT. Mice (WT, LCAT‐Tg, and LCAT‐KO, males, n = 5 per group) were fasted for 4‐6 hours and then bled by retro‐orbital sinus blood collection (~75‐100 μL). Mice were bled before, 1, 2, 3, and 4 days after ANIT gavage via the retro‐orbital sinus. Hepatic function markers, Total Bilirubin (A), Direct Bilirubin (B), Indirect Bilirubin (C), ALT (D), AST (E), and alkaline phosphatase (F.) were measured as described in the section. * P <.05 compared to WT and LCAT‐Tg mice, # P <.05 compared to LCAT‐Tg mice

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques:

    Change in plasma lipid and lipoproteins following ANIT treatment. Mice (WT, LCAT‐Tg, and LCAT‐KO, males, n = 4 per group) were fasted for 4‐6 hours and then bled by retro‐orbital sinus blood collection (~75‐100 μL). Mice were bled before, 1, 2, and 3 days after ANIT gavage via the retro‐orbital sinus, until peak levels of Lp‐X were present. Total Cholesterol (A), Free Cholesterol (B), Triglycerides (C), Phospholipids (D), Cholesteryl Ester (E) were measured as described in the section. (F) surface/core lipid ratio, was calculated following the formula (FC + PL)/(CE + TG). (G) LCAT activity, was measured using endogenous substrate and calculated as described in the section; red line represents the LCAT‐Tg activity (red legend, right, red x ‐axis) while blue and black lines represent LCAT‐KO and control mice, respectively (black legend, left x ‐axis). * P< .05 increase over baseline, # P <.05 decrease over baseline

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Change in plasma lipid and lipoproteins following ANIT treatment. Mice (WT, LCAT‐Tg, and LCAT‐KO, males, n = 4 per group) were fasted for 4‐6 hours and then bled by retro‐orbital sinus blood collection (~75‐100 μL). Mice were bled before, 1, 2, and 3 days after ANIT gavage via the retro‐orbital sinus, until peak levels of Lp‐X were present. Total Cholesterol (A), Free Cholesterol (B), Triglycerides (C), Phospholipids (D), Cholesteryl Ester (E) were measured as described in the section. (F) surface/core lipid ratio, was calculated following the formula (FC + PL)/(CE + TG). (G) LCAT activity, was measured using endogenous substrate and calculated as described in the section; red line represents the LCAT‐Tg activity (red legend, right, red x ‐axis) while blue and black lines represent LCAT‐KO and control mice, respectively (black legend, left x ‐axis). * P< .05 increase over baseline, # P <.05 decrease over baseline

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Clinical Proteomics, Activity Assay, Control

    Plasma lipoproteins by agarose gel electrophoresis. Plasma was obtained from mice (WT, n = 3, LCAT‐Tg, n = 3and LCAT‐KO, n = 3, males) either before (Baseline) or 1, 2, or 3 days after ANIT treatment (a single gavage of 100 mg/kg). 10 μL of plasma were loaded onto duplicate agarose gels followed by electrophoresis for 1 hour at 100 V. Gels were stained with Sudan Black (upper panels) or Filipin (lower panels) as described in section. 10 μL of purified human LDL, VLDL, and HDL were included as standards loaded on the left side of each gel. Lp‐X can be seen as backwards‐running (ie cathode‐migrating) fluorescent material by Filipin staining. The origin (point of application) is marked by a red arrow at the left of the gels and by a thin blue line running across the center of the gels. Vertical red lines to the left of the gels mark the regions where HDL, VLDL, LDL, and Lp‐X migrate. HDL, LDL, and VLDL migrate towards the anode (+) and Lp‐X migrates toward the cathode (−)

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Plasma lipoproteins by agarose gel electrophoresis. Plasma was obtained from mice (WT, n = 3, LCAT‐Tg, n = 3and LCAT‐KO, n = 3, males) either before (Baseline) or 1, 2, or 3 days after ANIT treatment (a single gavage of 100 mg/kg). 10 μL of plasma were loaded onto duplicate agarose gels followed by electrophoresis for 1 hour at 100 V. Gels were stained with Sudan Black (upper panels) or Filipin (lower panels) as described in section. 10 μL of purified human LDL, VLDL, and HDL were included as standards loaded on the left side of each gel. Lp‐X can be seen as backwards‐running (ie cathode‐migrating) fluorescent material by Filipin staining. The origin (point of application) is marked by a red arrow at the left of the gels and by a thin blue line running across the center of the gels. Vertical red lines to the left of the gels mark the regions where HDL, VLDL, LDL, and Lp‐X migrate. HDL, LDL, and VLDL migrate towards the anode (+) and Lp‐X migrates toward the cathode (−)

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Clinical Proteomics, Agarose Gel Electrophoresis, Electrophoresis, Staining, Purification

    Densitometric quantification of Lp‐X in Filipin stained gels. The fluorescent cathode‐migrating Lp‐X signal for samples on each gel were normalized to the fluorescent purified LDL signal on each gel to ensure accurate comparisons between gels. Average Lp‐X intensities (normalized to LDL) for each mouse line plus minus 1 SD are shown as a function of days after the ANIT treatment. WT; n = 3, LCAT‐KO; n = 3 and LCAT‐Tg; n = 3

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Densitometric quantification of Lp‐X in Filipin stained gels. The fluorescent cathode‐migrating Lp‐X signal for samples on each gel were normalized to the fluorescent purified LDL signal on each gel to ensure accurate comparisons between gels. Average Lp‐X intensities (normalized to LDL) for each mouse line plus minus 1 SD are shown as a function of days after the ANIT treatment. WT; n = 3, LCAT‐KO; n = 3 and LCAT‐Tg; n = 3

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Staining, Purification

    Lp‐X in WT and LCAT‐KO mouse liver. Transmission electron microscopy reveals the appearance of multilamellar Lp‐X in WT and LCAT‐KO mouse liver compartments. Lp‐X is taken up by Kupffer cells in WT (A, n = 40 slices) and LCAT‐KO (C, n = 12 slices) mouse liver and is seen in hepatic sinusoids of LCAT‐KO mice (E). Regions denoted by white boxes in (A), (C), and (E) are shown at higher magnification in (B), (D), and (F), respectively. Scale bars: (A): 2 μm; (B) 600 nm; (C): 800 nm; (D): 400 nm; (E): 1 μm; (F): 500 nm

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Lp‐X in WT and LCAT‐KO mouse liver. Transmission electron microscopy reveals the appearance of multilamellar Lp‐X in WT and LCAT‐KO mouse liver compartments. Lp‐X is taken up by Kupffer cells in WT (A, n = 40 slices) and LCAT‐KO (C, n = 12 slices) mouse liver and is seen in hepatic sinusoids of LCAT‐KO mice (E). Regions denoted by white boxes in (A), (C), and (E) are shown at higher magnification in (B), (D), and (F), respectively. Scale bars: (A): 2 μm; (B) 600 nm; (C): 800 nm; (D): 400 nm; (E): 1 μm; (F): 500 nm

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Transmission Assay, Electron Microscopy

    Recombinant human LCAT injection reduces Lp‐X in cholestatic murine plasma. FPLC analysis of WT mouse plasma at baseline (A and B), on day 3 after ANIT gavage (C and D) and on day 3 after ANIT gavage with multiple injections of rhLCAT in vivo (E and F). One hundred and fifty microliters of mouse plasma were separated through two Superose 6 columns in series producing 60 (0.5 mL each) fractions. Each fraction was analyzed for its cholesterol (total [TC] or unesterified [FC]) and phospholipid [PL] content as described in section. LDL, VLDL, and HDL migrate toward the anode (+, top) and Lp‐X migrates toward the cathode (−, bottom; B, D, and F). Typically, VLDL elutes in fractions 8‐22, LDL elutes in fractions 23‐32 and HDL elutes in fractions 35‐60 (A, C, and E). (A, C, E) illustrates the TC, FC, and PL profile of a WT mouse (A), WT mouse plasma on day 3 after ANIT gavage (C) and WT mouse plasma on day 3 after ANIT gavage followed by multiple in vivo injections of rhLCAT (E). (B, D, F) illustrates the corresponding migration of fractions 8‐32 (VLDL and LDL) on an agarose gel stained with Filipin as described in Figure . Lp‐X is visible in fractions 15‐35 on C and below the red (origin, point of application) line in D

    Journal: Pharmacology Research & Perspectives

    Article Title: LCAT protects against Lipoprotein‐X formation in a murine model of drug‐induced intrahepatic cholestasis

    doi: 10.1002/prp2.554

    Figure Lengend Snippet: Recombinant human LCAT injection reduces Lp‐X in cholestatic murine plasma. FPLC analysis of WT mouse plasma at baseline (A and B), on day 3 after ANIT gavage (C and D) and on day 3 after ANIT gavage with multiple injections of rhLCAT in vivo (E and F). One hundred and fifty microliters of mouse plasma were separated through two Superose 6 columns in series producing 60 (0.5 mL each) fractions. Each fraction was analyzed for its cholesterol (total [TC] or unesterified [FC]) and phospholipid [PL] content as described in section. LDL, VLDL, and HDL migrate toward the anode (+, top) and Lp‐X migrates toward the cathode (−, bottom; B, D, and F). Typically, VLDL elutes in fractions 8‐22, LDL elutes in fractions 23‐32 and HDL elutes in fractions 35‐60 (A, C, and E). (A, C, E) illustrates the TC, FC, and PL profile of a WT mouse (A), WT mouse plasma on day 3 after ANIT gavage (C) and WT mouse plasma on day 3 after ANIT gavage followed by multiple in vivo injections of rhLCAT (E). (B, D, F) illustrates the corresponding migration of fractions 8‐32 (VLDL and LDL) on an agarose gel stained with Filipin as described in Figure . Lp‐X is visible in fractions 15‐35 on C and below the red (origin, point of application) line in D

    Article Snippet: Recombinant human LCAT (rhLCAT) (MEDI6012) was provided by MedImmune, Gaithersburg, MD, USA and utilized as described in Figure .

    Techniques: Recombinant, Injection, Clinical Proteomics, In Vivo, Migration, Agarose Gel Electrophoresis, Staining