S-Adenosylhomocysteine targets methyltransferases by acting as a product inhibitor of SAM-dependent methylation reactions. Elevated levels of SAH can disrupt normal methylation activities, affecting DNA, proteins, and lipids, which may contribute to various diseases, including cardiovascular and neurodegenerative disorders. SAH is also an inhibitor for the METTL3-METTL14 heterodimer complex, which is involved in N6-methyladenosine (m6A) RNA methylation, with an IC50 of 0.9 μM.

In vitro, S-adenosylhomocysteine acts as a regulator of methyltransferases by inhibiting methylation processes. It is an inhibitor for the METTL3-METTL14 heterodimer complex with an IC50 of 0.9 μM. SAH binds to dsDNA as a methyltransferase inhibitor, which leads to DNA methylation and inhibits DNA binding. As an amino acid derivative and an intermediate in the synthesis of cysteine and adenosine, SAH modulates several metabolic pathways.

In vivo, S-adenosylhomocysteine plays a crucial role in cellular metabolism as a regulator of methylation processes. Elevated levels of SAH can disrupt normal methylation activities, affecting DNA, proteins, and lipids, which may contribute to various diseases, including cardiovascular and neurodegenerative disorders. Its involvement in regulating epigenetic processes makes SAH a key molecule in studies focused on methylation-dependent biological functions and disease mechanisms.

S-Adenosylhomocysteine is not typically evaluated in standard enzyme/receptor binding assays because it is an endogenous metabolite. However, its inhibition of methyltransferases can be assessed using enzyme activity assays. In these assays, a methyltransferase enzyme is incubated with its substrate and SAM in the presence of varying concentrations of SAH, and the extent of methylation is measured. The IC50 for inhibition of methyltransferase activity is determined from dose-response curves.

S-Adenosylhomocysteine is an endogenous metabolite and is not typically evaluated in cellular assays for drug discovery purposes. However, its effects on methylation can be studied in cell culture models. Cells are treated with SAH or compounds that modulate SAH levels, and global methylation levels are assessed. The compound's role as a METTL3-METTL14 inhibitor can be studied by measuring m6A RNA methylation levels in cells treated with SAH.

S-Adenosylhomocysteine is an endogenous metabolite and is not typically evaluated in animal experiments for therapeutic purposes. However, animal models may be used to study the effects of altered SAH levels on methylation and disease. Mice or rats with genetic or dietary modifications that affect SAH levels are studied to understand the role of methylation in various diseases, including cardiovascular and neurodegenerative disorders.

S-Adenosylhomocysteine has a molecular weight of 384.41 and a molecular formula of C14H20N6O5S. The compound has a melting point >175°C (dec.). It should be stored at -20°C. The compound is supplied at ≥95% purity. Detailed pharmacokinetic parameters are not relevant because SAH is an endogenous metabolite rather than a drug. SAH is formed as a byproduct of methylation reactions and is metabolized by SAH hydrolase to homocysteine and adenosine.

S-Adenosylhomocysteine is an endogenous metabolite and is not associated with toxicity at physiological concentrations. Elevated levels of SAH can disrupt normal methylation activities and may contribute to various diseases. As a research compound, SAH is generally considered safe at the concentrations used for laboratory studies. Standard safety precautions should be followed when handling the compound.

S-Adenosyl-L-homocysteine is an organosulfur compound, an S-adenosyl derivative of L-homocysteine. It has multiple functions, including acting as a cofactor, an inhibitor of EC 2.1.1.79 (cyclopropane-fatty acyl-phospholipid synthase), an inhibitor of EC 2.1.1.72 [site-specific DNA methyltransferase (adenine-specific)], a basic metabolite, and an epitope. It belongs to the adenosine class, organosulfur class, homocysteine derivative class, and homocysteine class. It is the conjugate acid of S-adenosyl-L-homocysteine and also the zwitterion tautomer of S-adenosyl-L-homocysteine. 5'-S-(3-amino-3-carboxypropyl)-5'-thioadenosine is generated from S-adenosylmethionine via transmethylation. S-adenosylhomocysteine is a metabolite present in or produced by Escherichia coli (K12 strain, MG1655 strain).
S-Adenosyl-L-homocysteine has been reported to exist in Daphnia frenulum, Drosophila melanogaster, and other organisms with relevant data.
S-Adenosylhomocysteine is an amino acid derivative and an intermediate in the synthesis of cysteine and adenosine. S-Adenosylhomocysteine (SAH) is formed after S-adenosylmethionine (SAM)-dependent methylation (homocysteine-methionine cycle) in biomolecules such as DNA, RNA, and proteins. Subsequently, it is hydrolyzed by S-adenosylhomocysteine hydrolases to produce adenosine and homocysteine. Because SAH regulates the methylation-dependent reaction, SAH levels and the SAH/SAM ratio can be used to assess the methylation status of macromolecules.
S-Adenosylhomocysteine (AdoHcy) is a direct precursor to all homocysteine in the body. This reaction is catalyzed by S-adenosylhomocysteine hydrolases and is reversible, with the equilibrium favoring the formation of AdoHcy. In vivo, the action of adenosine deaminase drives the reaction toward homocysteine production. This enzyme converts adenosine, the second product of the S-adenosine homocysteine hydrolase reaction, into inosine. Except for the methyl transfer of betaine and methylcobalamin in the methionine synthase reaction, all methylation reactions using S-adenosine methionine (AdoMet) as a methyl donor produce AdoHcy. Methylation plays a crucial role in the epigenetic regulation of protein expression through DNA and histone methylation. The inhibition of these AdoMet-mediated processes by AdoHcy has been shown to be a mechanism of metabolic alteration. Because the conversion of AdoHcy to homocysteine is reversible and the equilibrium favors AdoHcy production, elevated plasma homocysteine levels are usually accompanied by elevated AdoHcy levels. Many neurodegenerative diseases, such as dementia, depression, or Parkinson's disease, have reported transmethylation pathway disorders characterized by abnormalities in S-adenosine methionine, S-adenosine homocysteine, or their ratios. (A3511, A3512). 5'-S-(3-amino-3-carboxypropyl)-5'-thioadenosine. Formed by transmethylation of S-adenosylmethionine.
S-Adenosylhomocysteine is a naturally occurring amino acid derivative and an intermediate in the synthesis of cysteine and adenosine. It is formed as a byproduct of SAM-dependent methylation reactions and serves as a regulator of methyltransferases by inhibiting methylation processes. SAH is an inhibitor for the METTL3-METTL14 heterodimer complex with an IC50 of 0.9 μM. Its involvement in regulating epigenetic processes makes it a key molecule in studies focused on methylation-dependent biological functions and disease mechanisms. SAH is a research compound and is not used as a therapeutic agent.

C14H20N6O5S

384.41

384.121

979-92-0

439155

White to off-white solid powder

1.9±0.1 g/cm3

787.5±70.0 °C at 760 mmHg

209 - 211 °C

430.0±35.7 °C

0.0±2.9 mmHg at 25°C

1.839

0.15

5

11

7

26

504

5

O[C@@H]1[C@H](O)[C@@H](CSCC[C@H](N)C(=O)O)O[C@H]1N1C=NC2C(=NC=NC1=2)N

ZJUKTBDSGOFHSH-WFMPWKQPSA-N

InChI=1S/C14H20N6O5S/c15-6(14(23)24)1-2-26-3-7-9(21)10(22)13(25-7)20-5-19-8-11(16)17-4-18-12(8)20/h4-7,9-10,13,21-22H,1-3,15H2,(H,23,24)(H2,16,17,18)/t6-,7+,9+,10+,13+/m0/s1

(2S)-2-amino-4-[[(2S,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methylsulfanyl]butanoic acid

S-Adenosylhomocysteine; S-Adenosyl-L-homocysteine

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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