Hemin

Research use only, not for human use.

Hemin, a physiological erythroid maturation stimulator, is able to induce the expression of critical autophagic genes (Map1a1b (LC3), Beclin-1 gen, Atg5) in an erythroleukemia cell type.

Hemin, a physiological erythroid maturation stimulator, is able to induce the expression of critical autophagic genes (Map1a1b (LC3), Beclin-1 gen, Atg5) in an erythroleukemia cell type; increases the size of autophagic vacuoles and induces mitophagy in K562 cells; a heme oxygenase (HO)?1 inducer.(In Vitro):Hemin and PGJ2, used as positive controls, strongly increase both expression and activity of HMOX after 4 and 12 h, respectively. Indeed, a significant effect is found of 30 μM Hemin on cell proliferation in all used cell lines after 48 h, which is dose-dependent. Hemin treatment decreases cell proliferation to 62±5 %, 51±3 %, and 38±8 % in PA-TU-8902, BxPC-3 and MiaPaCa-2 cancer cells, respectively, with p<0.0001 for all comparisons. Furthermore, enhancement of anti-proliferative effects of statins is observed by Hemin, documented as decreased cell proliferation after 48 h of co-treatment. (In Vivo):Following the i.p. administration of Hemin (100 μmol/kg), the HO-1 level in the renal cortex begins to increase gradually. The HO-1 level reaches its peak 24 h after Hemin preconditioning. HO-1 is expressed mainly in the renal tubules. The HO-2 level in the kidney does not change following Hemin preconditioning.

Hemin and PGJ2, used as positive controls, strongly increase both expression and activity of HMOX after 4 and 12 h, respectively. Indeed, a significant effect is found of 30 μM Hemin on cell proliferation in all used cell lines after 48 h, which is dose-dependent. Hemin treatment decreases cell proliferation to 62±5 %, 51±3 %, and 38±8 % in PA-TU-8902, BxPC-3 and MiaPaCa-2 cancer cells, respectively, with p<0.0001 for all comparisons. Furthermore, enhancement of anti-proliferative effects of statins is observed by Hemin, documented as decreased cell proliferation after 48 h of co-treatment.

Following the i.p. administration of Hemin (100 μmol/kg), the HO-1 level in the renal cortex begins to increase gradually. The HO-1 level reaches its peak 24 h after Hemin preconditioning. HO-1 is expressed mainly in the renal tubules. The HO-2 level in the kidney does not change following Hemin preconditioning.

Hemin chloride

Autophagy

Autophagy

Autophagy

Cardiovascular Disease

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16009-13-5

651.9403

C34H32ClFeN4O4

>98% (HPLC)

DMSO: 6.6 mg/mL

CC1=C(CCC(O)=O)/C2=C/C3=C(CCC(O)=O)C(C)=C(/C=C4C(C)=C(C=C)C(/C=C5C(C)=C(C=C)C(/C=C1\[N-]2)=N/5)=N/4)[N-]3.[Fe+3]

Ferrate(2-), chloro[7,12-diethenyl-3,8,13,17-tetramethyl-21H,23H-porphine-2,18-dipropanoato(4-)-κN21,κN22,κN23,κN24]-, hydrogen (1:2), (SP-5-13)-

(-20℃)

With Ice Pack

≥ 2 years