AgingResearch.NewsJoin free

HL156A

HL156A has been studied in 1 paper since 2018: none in people yet, 1 in animals. The research so far is in animals. The newest paper, Sep 16, 2018: “Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice”.

Intervention

1 paper studies it6 findingsUpdated

PubChemMeSH

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

  • 1 lab
  • Animals1

What did studies of HL156A find?

6

Studies of HL156A measured 6 outcomes; the most studied are calcification (1 study), survival (1) and GSH/GSSG ratio (1).

Calcification

downin mice1

1 study

  1. HL156A decreases calcification in mice.

    “In histological sections, HL156A administered SAMP1/kl-/- mice exhibited a decrease in excessive calcification.”

    AnimalsSAMP1/kl-/-

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

Survival

upin mice1

1 study

  1. HL156A increases survival in mice.

    “treating SAMP1/kl-/- mice with HL156A (30 mg/kg) for 4 weeks improved survival”

    AnimalsSAMP1/kl-/-30 mg/kg4 weeks

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

GSH/GSSG ratio

upin mice1

1 study

  1. HL156A increases GSH/GSSG ratio in mice.

    “HL156A increased the GSH/GSSG ratio in the kidneys of SAMP1/kl-/- mice (8-12 weeks old).”

    AnimalsSAMP1/kl-/-kidney

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

More on GSH/GSSG ratio

Mitochondrial transmembrane potential

upin mouse cells1

1 study

  1. HL156A increases mitochondrial transmembrane potential in mouse cells.

    “Treatment of HL156A decreased reactive oxygen species production and enhanced mitochondrial transmembrane potential in SAMP1/kl-/- MEFs.”

    CellsSAMP1/kl-/-mouse embryonic fibroblast

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

More on Mitochondrial transmembrane potential

Reactive oxygen species production

downin mouse cells1

1 study

  1. HL156A decreases reactive oxygen species production in mouse cells.

    “Treatment of HL156A decreased reactive oxygen species production and enhanced mitochondrial transmembrane potential in SAMP1/kl-/- MEFs.”

    CellsSAMP1/kl-/-mouse embryonic fibroblast

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

More on Reactive oxygen species production

FoxO1 expression

upin mouse cells1

1 study

  1. HL156A increases FoxO1 expression in mouse cells.

    “HL156A induced FOXO1 expression through inhibition of the IGF-1/AKT/mTOR signaling pathways.”

    CellsSAMP1/kl-/-mouse embryonic fibroblast

    Antioxidant modifications induced by the new metformin derivative HL156A regulate metabolic reprogramming in SAMP1/kl (-/-) mice

    Aging

More on FoxO1 expression

Latest

Related