product name Related products
Description: 5-hydroxymethyl tolterodine (also known as Desfesoterodine, PNU 200577, 5-HMT, 5-HM) is a novel muscarinic receptor antagonist with Kb of 0.84 nM. It is a major pharmacologically active metabolite of tolterodine. 5-hydroxymethyl tolterodine produces a competitive and concentration-dependent inhibition of carbachol-induced contraction of guinea-pig isolated urinary bladder strips. 5-hydroxymethyl tolterodine antagotizes muscarinic receptors with a pA2 of 9.1.
References: Pharmacol Toxicol. 1997 Oct;81(4):169-72.
341.49
Formula
C22H31NO2
CAS No.
207679-81-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 68 mg/mL (199.1 mM)
Water: <1 mg/mL
Ethanol: 68 mg/mL (199.1 mM)
Solubility (In vivo)
Synonyms
Desfesoterodine, PNU 200577, 5-HMT, 5-HM
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390525
| In Vitro |
In vitro activity: 5-hydroxymethyl tolterodine is a major pharmacologically active metabolite of tolterodine. 5-hydroxymethyl tolterodine produces a competitive and concentration-dependent inhibition of carbachol-induced contraction of guinea-pig isolated urinary bladder strips. 5-hydroxymethyl tolterodine antagotizes muscarinic receptors with a pA2 of 9.1. 5-hydroxymethyl tolterodine causes a concentration-dependent inhibition of (-)3 H-QNB binding in homogenates of guinea-pig urinary bladder, parotid gland, heart and cerebral cortex. 5-hydroxymethyl tolterodine has a similar pharmacological profile with tolterodine. Intravenous infusion of 5-hydroxymethyl tolterodine produces a dose-dependent inhibition of the intravesical volume-induced urinary bladder contraction measured as the micturition pressure. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | 5-hydroxymethyl tolterodine is significantly more potent at inhibiting acetylcholine-induced urinary bladder contraction than electrically induced salivation in the anaesthetised cat (ID50 15 and 40 nmol/kg, respectively. 5-hydroxymethyl tolterodine is three times more potent at the urinary bladder compared to the salivary gland. |
| Animal model | Male guinea-pigs |
| Formulation & Dosage | Dissolved in saline; 2 nmol/kg -203 nmol/kg; i.v. injection |
| References | Pharmacol Toxicol. 1997 Oct;81(4):169-72. |
Related Posts
product name Related products
Description: Succinylcholine (also known as Suxamethonium Chloride Dihydrate) is a quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.
References: Anesthesiology. 2006 Apr;104(4):724-33.
397.34
Formula
C14H30N2O4.2Cl.2H2O
CAS No.
6101-15-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 79 mg/mL (198.8 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
Suxamethonium Chloride Dihydrate
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19391030
| In Vitro |
In vitro activity: Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References |
Related Posts
product name Related products
Description: Noradrenaline bitartrate monohydrate (also known as Levophed) is a direct alpha-adrenergic receptors stimulator. Noradrenaline modulates the gain of evoked activity, especially in sensory areas. Noradrenaline promotes long-term synaptic plasticity, in addition to these data emphasizing its short-term influence. Noradrenaline would signal ‘gross changes in the environment that produce sensory information strongly violating top-down expectations’ and would, through an enhancement of ‘bottom-up’ information processing at the expense of irrelevant ‘top-down’ expectations, favor behavioral adjustment.
References: Trends Neurosci. 2005 Nov;28(11):574-82.; Int Clin Psychopharmacol. 2003 Jul;18(4):191-202.
337.28
Formula
C8H11NO3.C4H6O6.H2O
CAS No.
108341-18-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 64 mg/mL (189.7 mM)
Water: 64 mg/mL (189.7 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
Levophed
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19398188
| In Vitro |
In vitro activity: Noradrenaline modulates the gain of evoked activity, especially in sensory areas. Noradrenaline promotes long-term synaptic plasticity, in addition to these data emphasizing its short-term influence. Noradrenaline would signal ‘gross changes in the environment that produce sensory information strongly violating top-down expectations’ and would, through an enhancement of ‘bottom-up’ information processing at the expense of irrelevant ‘top-down’ expectations, favor behavioral adjustment. Noradrenaline modulates drive and energy and exerts a fine regulation of specific processes including learning, memory, sleep, arousal and adaptation. Noradrenaline system is intimately involved in a range of psychological processes which, when disrupted, lead to the expression of classifiable psychiatric disorders. Noradrenaline appears to be involved in a range of psychological processes, including arousal (vigilance), cognition, learning and sleep regulation, and also in regulating response to stressors which might initiate or exacerbate depressive symptomatology. Noradrenaline deficiency in this pathway may reduce concentration, affect working memory and cause psychomotor retardation, resulting in apathy and depression,while an increase in noradrenaline in this pathway is predicted to alleviate poor concentration, apathy and depression. Noradrenaline effects are complex and depending on experimental conditions (ponto-medullary and medullary preparations) and species (rats or mice), exogenous Noradrenaline mainly facilitates or mainly inhibits the neonatal RRG, with a mixture of α1 facilitatory and α2 inhibitory effects. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Trends Neurosci. 2005 Nov;28(11):574-82.; Int Clin Psychopharmacol. 2003 Jul;18(4):191-202. |
Related Posts
product name Related products
Description: 5-hydroxymethyl tolterodine (also known as Desfesoterodine, PNU 200577, 5-HMT, 5-HM) is a novel muscarinic receptor antagonist with Kb of 0.84 nM. It is a major pharmacologically active metabolite of tolterodine. 5-hydroxymethyl tolterodine produces a competitive and concentration-dependent inhibition of carbachol-induced contraction of guinea-pig isolated urinary bladder strips. 5-hydroxymethyl tolterodine antagotizes muscarinic receptors with a pA2 of 9.1.
References: Pharmacol Toxicol. 1997 Oct;81(4):169-72.
341.49
Formula
C22H31NO2
CAS No.
207679-81-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 68 mg/mL (199.1 mM)
Water: <1 mg/mL
Ethanol: 68 mg/mL (199.1 mM)
Solubility (In vivo)
Synonyms
Desfesoterodine, PNU 200577, 5-HMT, 5-HM
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390525
| In Vitro |
In vitro activity: 5-hydroxymethyl tolterodine is a major pharmacologically active metabolite of tolterodine. 5-hydroxymethyl tolterodine produces a competitive and concentration-dependent inhibition of carbachol-induced contraction of guinea-pig isolated urinary bladder strips. 5-hydroxymethyl tolterodine antagotizes muscarinic receptors with a pA2 of 9.1. 5-hydroxymethyl tolterodine causes a concentration-dependent inhibition of (-)3 H-QNB binding in homogenates of guinea-pig urinary bladder, parotid gland, heart and cerebral cortex. 5-hydroxymethyl tolterodine has a similar pharmacological profile with tolterodine. Intravenous infusion of 5-hydroxymethyl tolterodine produces a dose-dependent inhibition of the intravesical volume-induced urinary bladder contraction measured as the micturition pressure. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | 5-hydroxymethyl tolterodine is significantly more potent at inhibiting acetylcholine-induced urinary bladder contraction than electrically induced salivation in the anaesthetised cat (ID50 15 and 40 nmol/kg, respectively. 5-hydroxymethyl tolterodine is three times more potent at the urinary bladder compared to the salivary gland. |
| Animal model | Male guinea-pigs |
| Formulation & Dosage | Dissolved in saline; 2 nmol/kg -203 nmol/kg; i.v. injection |
| References | Pharmacol Toxicol. 1997 Oct;81(4):169-72. |
Related Posts
product name Related products
Description: Succinylcholine (also known as Suxamethonium Chloride Dihydrate) is a quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for.
References: Anesthesiology. 2006 Apr;104(4):724-33.
397.34
Formula
C14H30N2O4.2Cl.2H2O
CAS No.
6101-15-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 79 mg/mL (198.8 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
Suxamethonium Chloride Dihydrate
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19391030
| In Vitro |
In vitro activity: Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References |
Related Posts
product name Related products
Description: Noradrenaline bitartrate monohydrate (also known as Levophed) is a direct alpha-adrenergic receptors stimulator. Noradrenaline modulates the gain of evoked activity, especially in sensory areas. Noradrenaline promotes long-term synaptic plasticity, in addition to these data emphasizing its short-term influence. Noradrenaline would signal ‘gross changes in the environment that produce sensory information strongly violating top-down expectations’ and would, through an enhancement of ‘bottom-up’ information processing at the expense of irrelevant ‘top-down’ expectations, favor behavioral adjustment.
References: Trends Neurosci. 2005 Nov;28(11):574-82.; Int Clin Psychopharmacol. 2003 Jul;18(4):191-202.
337.28
Formula
C8H11NO3.C4H6O6.H2O
CAS No.
108341-18-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 64 mg/mL (189.7 mM)
Water: 64 mg/mL (189.7 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
Levophed
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19398188
| In Vitro |
In vitro activity: Noradrenaline modulates the gain of evoked activity, especially in sensory areas. Noradrenaline promotes long-term synaptic plasticity, in addition to these data emphasizing its short-term influence. Noradrenaline would signal ‘gross changes in the environment that produce sensory information strongly violating top-down expectations’ and would, through an enhancement of ‘bottom-up’ information processing at the expense of irrelevant ‘top-down’ expectations, favor behavioral adjustment. Noradrenaline modulates drive and energy and exerts a fine regulation of specific processes including learning, memory, sleep, arousal and adaptation. Noradrenaline system is intimately involved in a range of psychological processes which, when disrupted, lead to the expression of classifiable psychiatric disorders. Noradrenaline appears to be involved in a range of psychological processes, including arousal (vigilance), cognition, learning and sleep regulation, and also in regulating response to stressors which might initiate or exacerbate depressive symptomatology. Noradrenaline deficiency in this pathway may reduce concentration, affect working memory and cause psychomotor retardation, resulting in apathy and depression,while an increase in noradrenaline in this pathway is predicted to alleviate poor concentration, apathy and depression. Noradrenaline effects are complex and depending on experimental conditions (ponto-medullary and medullary preparations) and species (rats or mice), exogenous Noradrenaline mainly facilitates or mainly inhibits the neonatal RRG, with a mixture of α1 facilitatory and α2 inhibitory effects. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Trends Neurosci. 2005 Nov;28(11):574-82.; Int Clin Psychopharmacol. 2003 Jul;18(4):191-202. |
Related Posts
product name Related products
Description: 6-Mercaptopurine Monohydrate (6-MP) is a widely used antileukemic agent and immunosuppressive drug that inhibits de novo purine synthesis through incorporation of thiopurine methyltransferase metabolites into DNA and RNA. Mercaptopurine is widely used to treat malignancies, rheumatic diseases, dermatologic conditions, inflammatory bowel disease, and solid organ transplant rejection. Mercaptopurine inhibits purine nucleotide synthesis and metabolism by inhibiting an enzyme called Phosphoribosyl pyrophosphate amidotransferase (PRPP Amidotransferase).
References: Eur J Clin Pharmacol. 2008 Aug;64(8):753-67; Am J Hum Genet. 1980 Sep;32(5):651-62.
170.19
Formula
C5H6N4OS
CAS No.
6112-76-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (587.6 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
6-MP
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19411616
| In Vitro |
In vitro activity: Mercaptopurine is widely used to treat malignancies, rheumatic diseases, dermatologic conditions, inflammatory bowel disease, and solid organ transplant rejection. Mercaptopurine inhibits purine nucleotide synthesis and metabolism by inhibiting an enzyme called Phosphoribosyl pyrophosphate amidotransferase (PRPP Amidotransferase). PRPP Amidotransferase is the rate limiting enzyme of purine synthesis. It alters the synthesis and function of RNA and DNA. Mercaptopurine interferes with nucleotide interconversion and glycoprotein synthesis. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Eur J Clin Pharmacol. 2008 Aug;64(8):753-67; Am J Hum Genet. 1980 Sep;32(5):651-62. |
Related Posts
product name Related products
Description: Mercaptopurine (also known as 6-Mercaptopurine, 6-MP) is a widely used antileukemic agent and immunosuppressive drug that inhibits de novo purine synthesis through incorporation of thiopurine methyltransferase metabolites into DNA and RNA. Mercaptopurine is widely used to treat malignancies, rheumatic diseases, dermatologic conditions, inflammatory bowel disease, and solid organ transplant rejection. Mercaptopurine inhibits purine nucleotide synthesis and metabolism by inhibiting an enzyme called Phosphoribosyl pyrophosphate amidotransferase (PRPP Amidotransferase).
References: Eur J Clin Pharmacol. 2008 Aug;64(8):753-67; Am J Hum Genet. 1980 Sep;32(5):651-62.
152.18
Formula
C5H4N4S
CAS No.
50-44-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 30 mg/mL (197.1 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
6-MP
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19412548
| In Vitro |
In vitro activity: Mercaptopurine is widely used to treat malignancies, rheumatic diseases, dermatologic conditions, inflammatory bowel disease, and solid organ transplant rejection. Mercaptopurine inhibits purine nucleotide synthesis and metabolism by inhibiting an enzyme called Phosphoribosyl pyrophosphate amidotransferase (PRPP Amidotransferase). PRPP Amidotransferase is the rate limiting enzyme of purine synthesis. It alters the synthesis and function of RNA and DNA. Mercaptopurine interferes with nucleotide interconversion and glycoprotein synthesis. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Eur J Clin Pharmacol. 2008 Aug;64(8):753-67; Am J Hum Genet. 1980 Sep;32(5):651-62. |
Related Posts
product name Related products
Description: Tegafur (also known as Fluorafur, FT-207, NSC 148958) is a chemotherapeutic 5-FU prodrug used in the treatment of cancers; It is a component of tegafur-uracil. When metabolized, it becomes 5-FU. T egafur-uracil is a formulated therapeutic oral agent consisting of a combination of the 5-fluorouracil (5-FU) congener prodrug tegafur (tetrahydrofuranyl-5-fluorouracil) and uracil (1:4).
References: Anticancer Res. 2015 Mar;35(3):1603-6.
200.17
Formula
C8H9FN2O3
CAS No.
17902-23-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 40 mg/mL (199.8 mM)
Water: 8 mg/mL (40 mM)
Ethanol: 7 mg/mL (35 mM)
Solubility (In vivo)
Synonyms
Fluorafur, FT-207, NSC 148958
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19413698
| In Vitro |
In vitro activity: Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References |
Related Posts
product name Related products
Description: Pramipexole 2HCl Monohydrate, a chemically novel dopamine agonist used for the treatment of Parkinsons disease symptoms, possesses antioxidant activity and is neuroprotective toward substantia nigral dopamine neurons in hypoxic-ischemic and methamphetamine models. Pramipexole reduces the levels of oxygen radicals produced by methylpyridinium ion (MPP+) both when incubated with SH-SY5Y cells and when perfused into rat striatum. Pramipexole also exhibits a concentration-dependent inhibition of opening of the mitochondrial transition pore induced by calcium and phosphate or MPP+.
References: J Neurochem. 1998 Jul;71(1):295-301; Eur J Pharmacol. 1992 May 14;215(2-3):161-70.
302.26
Formula
C10H17N3S.2HCl.H2O
CAS No.
191217-81-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 41 mg/mL (135.6 mM)
Water: 60 mg/mL (198.5 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19414405
| In Vitro |
In vitro activity: Pramipexole, a chemically novel dopamine agonist used for the treatment of Parkinsons disease symptoms, possesses antioxidant activity and is neuroprotective toward substantia nigral dopamine neurons in hypoxic-ischemic and methamphetamine models. Pramipexole reduces the levels of oxygen radicals produced by methylpyridinium ion (MPP+) both when incubated with SH-SY5Y cells and when perfused into rat striatum. Pramipexole also exhibits a concentration-dependent inhibition of opening of the mitochondrial transition pore induced by calcium and phosphate or MPP+. Pramipexole decreases the levels of dopamine metabolites dose dependently, whereas striatal dopamine levels remains unchanged. Pramipexole acts in both of these models to reduce the elevated dopamine turnover and the associated elevation in hydroxyl radical production secondary to increased MAO activity that could be responsible for oxidative damage to the nigrostriatal neurons. Pramipexole (4-100 mM) significantly attenuates DA- or L-DOPA-induced cytotoxicity and apoptosis, an action which is not blocked by D3 antagonist U-99194 A or D2 antagonist raclopride. Pramipexole also protects MES 23.5 cells from hydrogen peroxide-induced cytotoxicity in a dose-dependent manner. Pramipexole can effectively inhibit the formation of melanin, an end product resulting from DA or L-DOPA oxidation in cell-free system. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Pramipexole (0.001-1 mg/kg s.c.) reduces exploratory locomotor activity in mice. Pramipexole (1 mg/kg, p.o.) is able to significantly reduce the increased DA turnover, but by only 16%. |
| Animal model | |
| Formulation & Dosage | |
| References | J Neurochem. 1998 Jul;71(1):295-301; Eur J Pharmacol. 1992 May 14;215(2-3):161-70. |
Related Posts
product name Related products
Description: Pramipexole (also known as SND 919) is a potent dopamine agonist of the non-ergoline class that is used for the treatment of Parkinsons disease (PD) and restless legs syndrome (RLS). Pramipexole also possesses low/insignificant affinity (500-10,000 nM) for the 5-HT1A, 5-HT1B, 5-HT1D, and α2-adrenergic receptor. Pramipexole is a partial/full D2S, D2L, D3, D4 receptor agonist with a Ki of 3.9, 2.2, 0.5 and 5.1 nM for D2S, D2L, D3, D4 receptor, respectively.
References: Clin Ther. 2006 Aug;28(8):1065-78.
211.33
Formula
C10H17N3S
CAS No.
104632-26-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 42 mg/mL (198.7 mM)
Water: <1 mg/mL
Ethanol: 42 mg/mL (198.7 mM)
Solubility (In vivo)
Synonyms
SND 919
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19414454
| In Vitro |
In vitro activity: Pramipexole, a chemically novel dopamine agonist used for the treatment of Parkinsons disease symptoms, possesses antioxidant activity and is neuroprotective toward substantia nigral dopamine neurons in hypoxic-ischemic and methamphetamine models. Pramipexole reduces the levels of oxygen radicals produced by methylpyridinium ion (MPP+) both when incubated with SH-SY5Y cells and when perfused into rat striatum. Pramipexole also exhibits a concentration-dependent inhibition of opening of the mitochondrial transition pore induced by calcium and phosphate or MPP+. Pramipexole decreases the levels of dopamine metabolites dose dependently, whereas striatal dopamine levels remains unchanged. Pramipexole acts in both of these models to reduce the elevated dopamine turnover and the associated elevation in hydroxyl radical production secondary to increased MAO activity that could be responsible for oxidative damage to the nigrostriatal neurons. Pramipexole (4-100 mM) significantly attenuates DA- or L-DOPA-induced cytotoxicity and apoptosis, an action which is not blocked by D3 antagonist U-99194 A or D2 antagonist raclopride. Pramipexole also protects MES 23.5 cells from hydrogen peroxide-induced cytotoxicity in a dose-dependent manner. Pramipexole can effectively inhibit the formation of melanin, an end product resulting from DA or L-DOPA oxidation in cell-free system. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Pramipexole (0.001-1 mg/kg s.c.) reduces exploratory locomotor activity in mice. Pramipexole (1 mg/kg, p.o.) is able to significantly reduce the increased DA turnover, but by only 16%. |
| Animal model | |
| Formulation & Dosage | |
| References | J Neurochem. 1998 Jul;71(1):295-301; Eur J Pharmacol. 1992 May 14;215(2-3):161-70. |
Related Posts
product name Related products
Description: Edoxaban tosylate monohydrate (also known as DU-176b) is a potent, selective, orally bioavailable factor Xa inhibitor with Ki of 0.561 nM, >10 000-fold selectivity over thrombin and FIXa, and is used as an anticoagulant drug. Edoxaban acts as a direct factor Xa inhibitor. It was developed by Daiichi Sankyo and was approved in July 2011 in Japan for prevention of venous thromboembolisms (VTE) following lower-limb orthopedic surgery. It was also approved by the FDA in January 2015 for the prevention of stroke and non–central-nervous-system systemic embolism.
References: J Thromb Haemost. 2008 Sep;6(9):1542-9.
738.27
Formula
C24H30ClN7O4S.C7H8O3S.H2O
CAS No.
1229194-11-9
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (135.5 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
DU-176b
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19420069
| In Vitro |
In vitro activity: In human plasma, Edoxaban doubles prothrombin time and activates partial thromboplastin time at 0.256 and 0.508 μM, respectively. Kinase Assay: Cell Assay: Edoxaban tosylate monohydrate (DU-176b) inhibited FXa with Ki values of 0.561 nM for free FXa, 2.98 nM for prothrombinase, and exhibited >10 000-fold selectivity for FXa. DU-176b doubled prothrombin time and activated partial thromboplastin time in human plasma. DU-176b did not impair platelet aggregation by ADP, collagen or U46619 . |
|---|---|
| In Vivo | Oral administration of Edoxaban produces potent anti-Xa activity and high drug concentration in plasma in rats and monkeys. In vivo, Edoxaban dose-dependently inhibits thrombus formation in rat and rabbit thrombosis models. |
| Animal model | Venous stasis thrombosis model in rats and rabbits |
| Formulation & Dosage | Dissolved in 0.5% methylcellulose; 0.3–3 mg/kg (Rabbit); 0.5–12.5 mg/kg (Rat); oral gavage |
| References | J Thromb Haemost. 2008 Sep;6(9):1542-9. |
Related Posts
product name Related products
Description: Brompheniramine is a histamine H1 receptors antagonist that is commonly marketed as its salt brompheniramine maleate. It is readily available as an OTC drug and is indicated for the treatment of the symptoms of the common cold and allergic rhinitis, such as runny nose, itchy eyes, watery eyes, and sneezing. It is a first-generation antihistamine. Brompheniramine works by acting as an antagonist of histamine H1 receptors. It also functions as a moderately effective anticholinergic agent, and is likely an antimuscarinic agent similar to other common antihistamines such as diphenhydramine.
References: Prog Neuropsychopharmacol Biol Psychiatry. 2015 Jan 2;56:81-90; J Allergy Clin Immunol. 1982 Dec;70(6):458-64.
435.31
Formula
C16H19BrN2.C4H4
CAS No.
980-71-2
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 87 mg/mL (199.9 mM)
Water: 46 mg/mL (105.7 mM)
Ethanol: 18 mg/mL (41.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19427536
| In Vitro |
In vitro activity: Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References |
Related Posts
product name Related products
Description: Combretastatin A4 Phosphate (also known as CA4P, Fosbretabulin) Disodium is the water-soluble prodrug of Combretastatin A4 (CA4), which is a microtubule-targeting agent that binds β-tubulin with Kd of 0.4 μM in a cell-free assay. It is originally isolated from African tree Combretum caffrum. Combretastatin A4 inhibits the polymerization of tubulin with IC50 of 2.4 μM, and also disrupts tumor vasculature.
References: Br J Cancer. 1995 Apr;71(4):705-11; Cancer Res. 1997 May 15;57(10):1829-34.
440.29
Formula
C18H19O8P.2Na
CAS No.
168555-66-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 28 mg/mL (63.59 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Saline with a few drops of 5% Na2CO3: 30 mg/mL
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Fosbretabulin disodium (Combretastatin A-4 phosphate disodium, CA4P disodium) is the water-soluble prodrug of combretastatin A4 (CA4), which is originally isolated from African tree Combretum caffrum. CA4 is a tubulin-binding agent that binds at or near the colchicine binding site of β-tubulin (Kd = 0.40 μM), inhibits tubulin assembly with IC50 of 2.4 μM. CA4 is cytotoxic towards proliferating but not quiescent endothelial cells, has potent and selective toxicity towards tumor vasculature. CA4P (1 mM, 30 minutes) disrupts the endothelial microtubule cytoskeleton and mediates changes in endothelial cell morphology. CA4P stimulates actin stress fiber formation and membrane blebbing and increases monolayer permeability via Rho/Rho-kinase. CA4P increases endothelial cell permeability, while inhibiting endothelial cell migration and capillary tube formation predominantly through disruption of VE-cadherin/β-catenin/Akt signaling pathway, thereby leading to rapid vascular collapse and tumor necrosis. Kinase Assay: The assembly of microtubules from isolated tubulin is carried out spectrophotometrically at 350 nm and utilises the increase in turbidity which is associated with microtubule formation. Assembly is initiated by temperature increase from 10 to 35 °C. The effect of drugs on the increase in light absorption is carried. Drugs are dissolved in DMSO (<4%), which does not affect control assembly. Cell Assay: For the proliferation assay, the minimal concentration of FBS (1%) diluted in X-VIVO medium is used to allow sufficient viability of endothelial cells. After detachment, the cells are seeded at a concentration of 2×104 HUVECs in each well of 24-well plates, allowed to adhere overnight, and then incubated with or without cytokines (5 ng/ml FGF-2 or 5 ng/ml VEGF-A). CA4P is added at 0 – 50 nM. After incubation for 12, 24, 36, and 48 hours, cells are detached by trypsin/EDTA and manually counted using trypan blue exclusion. |
|---|---|
| In Vivo | CA4P causes rapid, extensive and irreversible vascular shutdown in experimental tumor models following the administration of a single dose at 10% of the maximum tolerated dose (MTD). CA4P causes a 93% reduction in vascular volume 6 h following drug administration. CA4P(100 mg/kg, 6 h following administration) reduces tumor blood by approximately 100-fold, compared with approximately 7-fold in the spleen. |
| Animal model | BD9 rats implanted with tumor |
| Formulation & Dosage | Dissolved in 0.9% saline with a few drops of 5% Na2CO3; 100 mg/kg, 3 ml/kg; i.p. injection |
| References | Br J Cancer. 1995 Apr;71(4):705-11; Cancer Res. 1997 May 15;57(10):1829-34. |
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Description: Monomethyl auristatin E (also known as MMAE) is a synthetic, potent antimitotic agent by blocking the polymerisation of tubulin, due to its toxicity, it cannot be used as a drug itself; instead, it is linked to a monoclonal antibody (MAB) which directs it to the cancer cells. In the marketed drug Brentuximab vedotin, the name vedotin refers to MMAE plus its linking structure to the antibody (Brentuximab). MMAE is a potent antimitotic drug derived from peptides occurring in marine shell-less mollusc Dolabella auricularia called dolastatins which show potent activity in preclinical studies, both in vitro and in vivo, against a range of lymphomas, leukemia and solid tumors. MMAE show potency of up to 200 times that of vinblastine, another antimitotic drug used for Hodgkin lymphoma as well as other types of cancer.
References: Blood. 2003 Aug 15;102(4):1458-65; Blood. 2009 Sep 24;114(13):2721-9.
717.98
Formula
C39H67N5O7
CAS No.
474645-27-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (139.3 mM)
Water: <1 mg/mL
Ethanol: 100 mg/mL (139.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: When coupled to cAC10, MMAE shows selective cytotoxicity in CD30+ cells, and induces G2/M-phase growth arrest and cell death through the induction of apoptosis. [1] When coupled to anti-CD79b antibody, anti–CD79b-vcMMAE has very potent and broad activity across a large panel of NHL cell lines in vitro. [2] When coupled to anti-HER2 antibody, hertuzumab-vc-MMAE can also be effectively internalized and potently kill HER2 over-expressing tumor cells. Kinase Assay: Cell Assay: Cytotoxicity is measured using Alamar Blue dye reduction assay according to the manufacturers directions. Briefly, a 40% solution (wt/vol) of Alamar Blue is freshly prepared in complete media just before cultures are added. Ninety-two hours after drug exposure, Alamar Blue solution is added to cells to constitute 10% culture volume. Cells are incubated for 4 hours, and dye reduction is measured on a Fusion HT fluorescent plate reader (Packard Instruments, Meriden, CT). Cell lines used: CD30+ Karpas 299 cells |
|---|---|
| In Vivo | The Karpas 299 ALCL model, cAC10-vcMMAE (1 mg/kg, i.v.) induces complete, durable tumor regression, while free MMAE (0.36 mg/kg) doesn’t produce detectable antitumor activity. In mouse xenograft models of NHL, anti–CD79b-vcMMAE (7 mg/kg, p.o.) strikingly results in sustained complete tumor remission. |
| Animal model | In vivo therapy tests were undertaken in athymic mice with subcutaneous L2987 human lung adenocarcinoma xenografts. MMAE conjugates were administered at 3 mg mAb component/kg/dose. All of the tested MMAE conjugates were highly efficacious, leading to long-term regressions of established tumors, whereas the nonbinding control conjugates had no effect on tumor growth. In addition, there were no apparent toxicities associated with conjugate treatment |
| Formulation & Dosage | |
| References | Blood. 2003 Aug 15;102(4):1458-65; Blood. 2009 Sep 24;114(13):2721-9; Nat Biotechnol. 2003 Jul;21(7):778-84. |
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Description: Disodium (R)-2-Hydroxyglutarate is a potent and competitive inhibitor of α-ketoglutarate-dependent dioxygenases with Ki of 0.628 mM. In U-87MG cells, (R)-2-Hydroxyglutarate acts as weak antagonists of α-KG to inhibit α-KG-dependent histone demethylases and increases dimethylation on both H3K9 and H3K79. Besides, (R)-2-Hydroxyglutarate inhibits ATP synthase and mTOR signaling, and thus causes growth arrest and tumor cell killing.
References: Cancer Cell. 2011 Jan 18;19(1):17-30; Cell Metab. 2015 Sep 1;22(3):508-15.
192.08
Formula
C5H6Na2O5
CAS No.
103404-90-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: <1 mg/mL
Water: 38 mg/mL (197.83 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: In U-87MG cells, (R)-2-Hydroxyglutarate acts as weak antagonists of α-KG to inhibit α-KG-dependent histone demethylases and increases dimethylation on both H3K9 and H3K79. Besides, (R)-2-Hydroxyglutarate inhibits ATP synthase and mTOR signaling, and thus causes growth arrest and tumor cell killing. Kinase Assay: To assay human JHDM1A/KDM2A demethylase activity toward H3K36me2, His tagged JHDM1A is first obtained by transforming pET28a-JHDM1A into Escherichia coli BL21 and protein expression is induced by addition of 1 mM IPTG at 30° C when cell density reaches 0.5 OD600 units. Cells are lysed by sonication and Ni-NTA agarose is used to purify His-JHDM1A fusion proteins. Histone demethylase assay is carried out by incubating 2 μg oligonucleosomes, 4 μg purified His-JHDM1A, and/or 10–50 mM L- or D-2-HG in histone demethylation buffer [50 mM HEPES (pH 8.0), 625 μM Fe(NH4)2(SO4)2, 0.1–0.5 mM α-KG, 2 mM ascorbate] at 37° C for 2–3 hr and the reactions are stopped by the addition of SDS loading buffer and subsequently analyzed by western blotting using anti-H3K36me2 antibody. To measure CeKDM7A demethylase activity toward H3K9me2 and H3K27me2, two synthetic dimethylated peptides H3K9me2 [ARTKQTARK (me2)STGGKA] and H3K27me2 [QLATKAARK (me2)SAPAS] are used as substrates. Demethylase assays are carried out in the presence of 10 μg enzyme, 1 μg peptide in 20 μl buffer 20 mM Tris-HCl (pH 7.5), 150 mM NaCl, 50 μM Fe(NH4)2(SO4)22, 100 μM α-KG, 2 mM Vc, 10 mM PMSF for 3 hr. The demethylation reaction mixture is desalted by passing through a C18 ZipTip. To examine the inhibitory effect of 2-HG, various concentrations of 2-HG are incubated with KDM7A briefly before adding other reaction mixtures. The samples are analyzed by a MALDI-TOF/TOF mass spectrometer. Cell Assay: Cells are seeded in 12-well plates and, after overnight incubation, treated with the indicated concentrations of each compound. After harvesting, cells are stained with acridine orange (AO) and 4′,6-diamidino-2-phenylindole (DAPI). Cell number and viability are measured based on AO and DAPI fluorescence as measured by NC3000 following the manufacturer’s instructions. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | Cancer Cell. 2011 Jan 18;19(1):17-30; Cell Metab. 2015 Sep 1;22(3):508-15. |
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Description: Sodium Tauroursodeoxycholate (TUDC) is a water soluble bile salt, which is used for the treatment of gallstones and liver cirrhosis. In vitro, Tauroursodeoxycholate shows protective and reversing effects on 17βEG-induced impairment of the cVA-of-CLF. In Mz-ChA-1 cholangiocarcinoma cells, Tauroursodeoxycholate inhibits cell growth via Ca2+-, PKC-, and MAPK-dependent pathways. In isolated rat hepatocytes, Tauroursodeoxycholate inhibits bile acid-Induced Apoptosis via a β1-integrin-mediated formation of cAMP.
References: J Hepatol. 2001 Feb;34(2):184-91; Eur J Pharmacol. 2001 Jun 1;421(1):55-60; Am J Physiol Gastrointest Liver Physiol. 2004 Jun;286(6):G973-82.
521.69
Formula
C26H44NNaO6S
CAS No.
35807-85-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (191.7 mM)
Water: 100 mg/mL (191.7 mM)
Ethanol: 71 mg/mL (136.1 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: In vitro, Tauroursodeoxycholate shows protective and reversing effects on 17βEG-induced impairment of the cVA-of-CLF. In Mz-ChA-1 cholangiocarcinoma cells, Tauroursodeoxycholate inhibits cell growth via Ca2+-, PKC-, and MAPK-dependent pathways. In isolated rat hepatocytes, Tauroursodeoxycholate inhibits bile acid-Induced Apoptosis via a β1-integrin-mediated formation of cAMP. Kinase Assay: Cell Assay: After trypsinization, Mz-ChA-1 cells are suspended in CCM at 5 × 104 cells/mL, and 200 μL of the cell suspension are seeded into flat-bottomed 96-well plates. After an initial incubation step of 4 h at 37°C in a 5% CO2 incubator, the cells are incubated at 37°C with TUDCA (0.2–200 μM). After incubation for 24–96 h, [3H]thymidine is put into each well at 5.0 μCi/mL and incubated for additional 4 h. [3H]thymidine incorporation is measured by a scintillation counter. At the end of each incubation period, cell viability is evaluated by trypan blue exclusion. |
|---|---|
| In Vivo | In phalloidin-induced cholestasis rats, Tauroursodeoxycholate (360 μmol/kg, i.v.) significantly suppresses the decrease in bile flow and increases in serum alkaline phosphatase, leucine aminopeptidase and glutamic pyruvic transaminase activities, cholesterol, phospholipid and bile acid concentrations. |
| Animal model | Phalloidin-induced cholestasis rats |
| Formulation & Dosage | Dissolved in saline; 360 μmol/kg; i.v. injection |
| References | J Hepatol. 2001 Feb;34(2):184-91; Eur J Pharmacol. 2001 Jun 1;421(1):55-60; Am J Physiol Gastrointest Liver Physiol. 2004 Jun;286(6):G973-82. |
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Description: Phosphoramidon Disodium Salt is a metalloendopeptidase inhibitor, which is widely used as a biochemical research tool. Phosphoramidon In porcine aortic endothelial cells, phosphoramidon (10-4 M) inhibited immunoreactive-endothelin (IR-ET) release by 10-20% and increased IR-CTF levels. These results suggested that phosphoramidon reduced the IR-ET release through affecting the conversion of big ET-1 to ET-l. In cultured endothelial cells, phosphoramidon inhibited the increase of ET-1 and C-terminal fragment (CTF) of big ET-1. However, phosphoramidon increased big ET-1 secretion
References: Biochem Biophys Res Commun. 1975;65:352-7; Surg Endosc. 2001;15:882-5; J Mol Neurosci. 2011;43(3):424-7.
588.48
Formula
C23H34N3Na2O10P
CAS No.
164204-38-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (169.9 mM)
Water: 100 mg/mL (169.9 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Phosphoramidon is a powerful inhibitor of thermolysin without inhibiting the other endopeptidases such as trypsin, papain, chymotrypsin. Phosphoramidon reduces tumor cell invasion in CC531 cells. Kinase Assay: Cell Assay: In cultured endothelial cells, phosphoramidon inhibited the increase of ET-1 and C-terminal fragment (CTF) of big ET-1. However, phosphoramidon increased big ET-1 secretion |
|---|---|
| In Vivo | In rats bearing colon carcinoma CC531 xenografts, Phosphoramidon (250 mg/Rat i.p.) significantly reduces tumor cell growth. Intranasal phosphoramidon increases beta-amyloid levels in wild-type and NEP/NEP2-deficient mice, and thus can be use to model Alzheimers disease (AD). |
| Animal model | WAG rats bearing colon carcinoma CC531 xenografts |
| Formulation & Dosage | Dissolved in 0.9% NaCl; 250 mg/Rat; i.p. injection |
| References | Biochem Biophys Res Commun. 1975 Jul 8;65(1):352-7; Surg Endosc. 2001 Aug;15(8):882-5; J Mol Neurosci. 2011 Mar;43(3):424-7. |
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Description: Meclofenoxate (also known as Centrophenoxine) HCl is an anti-aging drug used to treat the symptoms of senile dementia and Alzheimers disease, and also inhibits the activity of cholinephosphotransferase. Meclofenoxate hydrochloride, an ester of dimethylethanolamine (DMAE) and 4-chlorophenoxyacetic acid (pCPA), has been shown to improve memory, have a mentally stimulating effect, and improve general cognition.
References: Age Ageing. 1977 May;6(2):123-31.
294.17
Formula
C12H17Cl2NO3
CAS No.
3685-84-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 58 mg/mL (197.2 mM)
Water: 58 mg/mL (197.2 mM)
Ethanol:
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References |
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Description: Tenofovir Alafenamide (also known as TAF and GS-7340) is a novel prodrug of tenofovir, which is a reverse transcriptase inhibitor, used for the treatment of HIV and Hepatitis B. By blocking reverse transcriptase, Tenofovir Alafenamide prevent HIV from multiplying and can reduce the amount of HIV in the body. Tenofovir alafenamide is a prodrug that it is inactive in the parent form. In the body, tenofovir alafenamide is converted to tenofovir diphosphate (TFV-DP).
References: Nucleosides Nucleotides Nucleic Acids. 2001;20:1085-90; Antimicrob Agents Chemother. 2005;49:1898-906.
476.47
Formula
C21H29N6O5P
CAS No.
379270-37-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 95 mg/mL (199.4 mM)
Water: <1 mg/mL
Ethanol: 95 mg/mL (199.4 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: GS-7340 has a potent anti-HIV activity with IC50 of 0.005 μM. GS 7340 has a half-life of 90 min in human plasma and a half-life of 28.3 min in an MT-2 cell extract at 37°C. the hepatic uptake of GS-7340 isfacilitated by OATP1B1 and OATP1B3, respectively. GS-7340 inhibits HBV reverse transcriptase after being converted to the pharmacologically active form, TFV-DP. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | In male beagle dogs, GS 7340 (10 mg/kg, p.o.) results in an enhanced distribution to lymphatic tissue. |
| Animal model | |
| Formulation & Dosage | |
| References | Nucleosides Nucleotides Nucleic Acids. 2001 Apr-Jul;20(4-7):1085-90; Antimicrob Agents Chemother. 2005 May;49(5):1898-906. |