The primary mechanism of action of semicarbazide hydrochloride involves binding to copper or iron ions within cells. This metal binding activity is thought to mediate its antiviral, anti-infective, and antitumor effects. The compound may also act as a monoamine oxidase inhibitor. By chelating essential metal ions, semicarbazide hydrochloride may disrupt metal-dependent enzymatic processes in pathogens and cancer cells. Further research is needed to fully elucidate its molecular targets.

In vitro studies have demonstrated that semicarbazide hydrochloride possesses antiviral, anti-infective, and antineoplastic activities. The compound has been used as a starting material for the synthesis of semicarbazone derivatives with potential antiviral activity. Its activity is attributed to its ability to bind copper or iron in cells. The compound's effects on various cell lines and pathogens have been investigated, though specific potency data are limited in the available literature.

In vivo activity data for semicarbazide hydrochloride are limited in the published literature. The compound is primarily used as a chemical reagent and research tool rather than as a therapeutic agent. Some studies have explored its use in the synthesis of bioactive compounds. Animal model studies evaluating the in vivo efficacy of semicarbazide hydrochloride itself have not been extensively reported. Further investigations are needed to assess its in vivo pharmacological effects.

For metal binding studies, spectrophotometric or electrochemical methods are used to characterize the interaction between semicarbazide hydrochloride and metal ions such as copper or iron. For enzyme inhibition assays, monoamine oxidase activity is measured using standard fluorometric or colorimetric substrates. The compound is incubated with the enzyme and substrate, and product formation is monitored. IC₅₀ values are calculated from dose-response curves. For antiviral activity screening, standard plaque reduction or cytopathic effect assays are employed.

For in vitro cell-based studies, various cell lines may be used to evaluate the compound's cytotoxicity and antiviral activity. Cells are cultured in appropriate media and exposed to serial dilutions of semicarbazide hydrochloride. Cell viability is assessed using MTT, resazurin, or other viability assays. For antiviral assays, virus-infected cells are treated with the compound, and viral replication is quantified by plaque assay, qPCR, or immunofluorescence. Cytotoxicity and antiviral IC₅₀ values are determined.

In vivo animal studies for semicarbazide hydrochloride are limited. For related compounds, mouse models of infection or tumor xenografts may be used. Test compound is administered via oral, intraperitoneal, or intravenous routes. Efficacy endpoints include tumor growth inhibition, reduction in viral load, or survival. Standard protocols for in vivo efficacy studies are described in the literature and can be adapted for semicarbazide hydrochloride derivatives.

Absorption, Distribution and Excretion
...binds to cytosine residues in RNA, to deoxycytosine residues in DNA in vitro, and to cytosine and deoxycytosine nucleosides.

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Pharmacokinetic properties of semicarbazide hydrochloride have not been extensively characterized. As a small hydrophilic molecule with a molecular weight of 111.53 g/mol, it is expected to have rapid absorption and distribution. The compound is highly water-soluble. Specific PK parameters such as half-life, clearance, and protein binding have not been reported. The compound's metabolism and elimination pathways are not well documented. Further pharmacokinetic studies are needed.

Non-Human Toxicity Values
Oral LD50 in mice: 225 mg/kg
Intraperitoneal LD50 in mice: 145 mg/kg
Subcutaneous LD50 in mice: 167 mg/kg

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Toxicological data for semicarbazide hydrochloride are available from chemical safety databases. The compound is classified as a chemical hazard and should be handled with appropriate precautions. It may cause irritation to skin, eyes, and respiratory tract. Systemic toxicity data are limited. As a urea derivative, it may have a moderate toxicity profile. Standard toxicological assessments are needed for comprehensive safety evaluation.

[1]. Adam Becalski, et al. Semicarbazide Formation in Azodicarbonamide-Treated Flour: A Model Study. J Agric Food Chem. 2004 Sep 8;52(18):5730-4.

Snow-white crystals. Used as a reagent for ketones and aldehydes, it produces crystalline compounds with characteristic melting points. (EPA, 1998)
Aminourea hydrochloride is an organic molecular entity.
Mechanism of Action
Aminourea is a hydrazine derivative that is carcinogenic in mice, but has shown little or no mutagenicity in Salmonella microsomal assays. To elucidate whether the genotoxic mechanism leads to the non-mutagenic carcinogenicity of aminourea,… 32P-5'-tagged DNA fragments obtained from the c-Ha-ras-1 proto-oncogene and the p53 tumor suppressor gene were investigated to study aminourea-induced DNA damage. In the presence of Cu(II), aminourea frequently causes DNA damage at thymine and cytosine residues. Catalase and bartophenone partially inhibited DNA damage, indicating that hydrogen peroxide and Cu(I) are involved in DNA damage. High concentrations of aminourea in the presence of catalase induce DNA damage, particularly at the G site in the 5'-AG sequence, and less so at the 5'-G sites in the GG and GGG sequences. Electron paramagnetic resonance (EPR) spectroscopy confirmed that aminourea reacts with Cu(II) to generate carbamoyl radicals (·CONH2), which may originate from the nitrogen-centered radicals of aminourea. Azodicarbonamide also generates carbamoyl radicals and frequently induces DNA damage at the 5'-G sites in the GG and GGG sequences, indicating that carbamoyl radicals are involved in this sequence-specific DNA damage induced by aminourea. Based on previous reports, the sequence-specific DNA damage at the G site in the 5'-AG sequence in this study was caused by nitrogen-centered radicals. This study shows that aminourea induces DNA damage in the presence of Cu(II) by generating hydrogen peroxide and Cu(I). Furthermore, aminourea-derived radicals are also involved in DNA damage. The DNA damage induced by these active substances may be related to the carcinogenicity of aminourea.

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Semicarbazide hydrochloride is primarily used as a chemical reagent for the detection and characterization of carbonyl compounds. It is also used as a building block in organic synthesis for the preparation of semicarbazone and other derivatives. The compound has been studied for its potential biological activities including antiviral, anti-infective, and antineoplastic effects. No clinical trials or regulatory approvals as a therapeutic agent have been reported.

CH6CLN3O

111.5308

111.019

563-41-7

57-56-7 (Parent)

11236

Prisms from dilute alcohol
White crystals

1.286g/cm3

235.3ºC at 760 mmHg

175-177 °C (dec.)(lit.)

66.5ºC

0.0407mmHg at 25°C

1.121

4

2

0

6

42.2

0

Cl[H].O=C(N([H])[H])N([H])N([H])[H]

XHQYBDSXTDXSHY-UHFFFAOYSA-N

InChI=1S/CH5N3O.ClH/c2-1(5)4-3;/h3H2,(H3,2,4,5);1H

aminourea;hydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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

H2O : 100 mg/mL (896.62 mM)
DMSO : 100 mg/mL (896.62 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (22.42 mM) (saturation unknown) in 10% DMSO + 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 DMSO 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 (22.42 mM) (saturation unknown) in 10% DMSO + 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 DMSO 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 (22.42 mM) (saturation unknown) in 10% DMSO + 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 DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 50 mg/mL (448.31 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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