N'-Phenylacetohydrazide is a biochemical reagent that can be utilized in research pertaining to life sciences as an organic compound or biological material.

Interactions
This study investigated the alleviating effect of xylitol on acetylphenylhydrazine-induced hemolytic anemia in rabbits. Animal experiments used two different concentrations of xylitol solutions, 5% and 10%, with a total dose of 2 g/kg body weight and infusion rates of 10 mg/kg body weight/min and 20 mg/kg body weight/min, respectively. Acetylphenylhydrazine (APH) at two different concentrations (5 mg/kg and 10 mg/kg) was administered intraperitoneally to rabbits in different groups as a hemolysis inducer. All rabbits infused with xylitol showed a significant reduction in acute APH-induced hemolysis. Compared to the 10% xylitol solution, the 5% isotonic xylitol solution better maintained and restored hematological parameters (hematocrit, hemoglobin concentration, reduced glutathione (GSH) content, and reticulocyte count). Increased 51CR-labeled erythrocyte viability confirmed the beneficial effect of xylitol. After treatment with 10 mg/kg APH, the erythrocyte survival rate (expressed as chromium-labeled) of rabbits infused with 5% xylitol increased from approximately 33% (erythrocyte survival rate of rabbits injected with APH alone) to 67% of that of normal rabbits. Erythrocytes in the APH-treated group absorbed xylitol more readily than those in the control group. 1 mM ascorbic acid and α-mercaptopropionylglycine significantly (p<0.005) inhibited the formation of Heinz bodies in erythrocytes during acetylphenylhydrazine incubation, while cysteine, cysteamine, and methionine did not have this effect. The effect of ascorbic acid was concentration-dependent, with significant antioxidant activity at concentrations as low as 0.1 mM. This study investigated the effect of pteroylglutamate (PGA) on folate distribution during acetylphenylhydrazine (APH)-induced hemolysis. One group of rabbits received daily APH injections at a dose of 1 mL 2.5% solution/kg; the other group received 10 mg PGA three times daily concurrently with APH injections. Blood samples were collected for hematologic cell counting and folate activity assays. Animals were sacrificed on day 8, and folate activity in bone marrow and liver was analyzed using three different bioassays. Packed erythrocytes were incubated with radiolabeled PGA to measure uptake. As the reticulocyte cytosis induced by APH increased to 87% by day 7, erythrocyte folate activity gradually increased. Compared to the untreated control group, serum folate activity was normal, liver folate activity was slightly decreased, and bone marrow folate activity was increased. When rabbits were simultaneously treated with PGA, folate activity increased 2–5 times, with more significant increases in two of the three bioassays, but this was not observed when using the Pediococcus cerevisiae assay. Similar results were observed in the serum folate activity assay. All three bioassays showed that APH combined with PGA increased folate levels compared to APH alone, while liver folate levels differed significantly between the two control groups. When rabbits received only APH treatment, the average uptake of labeled PGA by packed erythrocytes was 2.7% of the folic acid content in the incubation solution; however, when rabbits received both APH and PGA treatment, this uptake was 0.72%. The study concluded that although hemolytic stimulation leads to significant folic acid transfer from the bone marrow, hematopoietic tissues can utilize more folic acid when supplemented with prostaglandin A (PGA) via parenteral administration. The reaction of oxyhemoglobin with acetylphenylhydrazine leads to hemoglobin denaturation and precipitation, influenced by hydrogen peroxide (H₂O₂) and superoxide anions (O₂⁻) generated during the reaction. Analysis of different hemoglobin oxidation products revealed that H₂O₂ accelerates overall hemoglobin breakdown by affecting the oxidation rate of oxyhemoglobin, while O₂⁻ inhibits overall hemoglobin breakdown. The addition of reduced glutathione (GSH) or ascorbic acid slowed the oxidation rate of oxyhemoglobin, the rate of O₂⁻ formation, and the overall rate of hemoglobin breakdown. These results are consistent with the generation mechanism of acetylphenylhydrazine radicals, and glutathione (GSH), ascorbic acid, and superoxide anion (O₂⁻) acted as free radical scavengers, preventing further reactions. The reaction produced bilirubin, acetylphenylhydrazine, and methemoglobin, which combined to form a hemichrome. This hemichrome was unstable and precipitated first. It was also less stable than the hemichrome formed by the direct reaction of acetylphenylhydrazine and methemoglobin, presumably because the methemoglobin formed from oxyhemoglobin and acetylphenylhydrazine was modified by free radicals and hydrogen peroxide (H₂O₂) generated in the reaction.

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Non-human toxicity values
Oral LD50 in mice: 270 mg/kg

1-Acetyl-2-phenylhydrazine is a colorless prismatic or white solid. (NTP, 1992)
APH is a member of the phenylhydrazine class of compounds.
Therapeutic Uses
/Previous Uses:/Treatment of polycythemia.

C8H10N2O

150.18

150.079

114-83-0

8247

Hexagonal prisms

1.143g/cm3

214.1ºC at 760mmHg

128-131 °C(lit.)

1E-06mmHg at 25°C

1.613

2

2

2

11

130

0

O=C(C([H])([H])[H])N([H])N([H])C1C([H])=C([H])C([H])=C([H])C=1[H]

UICBCXONCUFSOI-UHFFFAOYSA-N

InChI=1S/C8H10N2O/c1-7(11)9-10-8-5-3-2-4-6-8/h2-6,10H,1H3,(H,9,11)

N'-phenylacetohydrazide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Ethanol: 100 mg/mL (665.87 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (16.65 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (16.65 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (16.65 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)