6-keto-PGE1 (1 μg/mL; 30 min) can directly and stably isolate feline liver lysosomes and significantly reduce the release of β-glucuronidase and cathepsin D [1].

6-Keto-PGE1 (250 ng/kg/min; intravenous injection; continuous infusion; starting 15 minutes after trauma and continuing throughout the experimental period) significantly prolonged the survival time of rats with traumatic shock to 2.6 hours, while reducing plasma cathepsin D and MDF levels and stabilizing mean arterial blood pressure [1]. In healthy sham-operated rats, 6-Keto-PGE1 (250 ng/kg/min; intravenous injection; continuous infusion; 5 hours) moderately and continuously reduced mean arterial blood pressure (a total reduction of 23 mmHg after 5 hours) without affecting heart rate [1]. 6-Keto-PGE1 (1 μg/min; intra-arterial infusion) significantly reduced mesenteric perfusion pressure by approximately 27-31% and reversibly inhibited the vasoconstrictive response of the feline mesenteric vascular bed to sympathetic stimulation, norepinephrine, and angiotensin II [2]. 6-keto-PGE1 (0.3-10 μg; rapid intravenous injection) is a potent bronchodilator in a cat model of 5-hydroxytryptamine-induced bronchoconstriction. Its efficacy in reducing central airway resistance is 3-10 times that of PGI2, and it has very low pulmonary vasomotor activity. Its effect is independent of stimulation of the cyclooxygenase pathway [3].

Animal/Disease Models:Sprague-Dawley rats (male, 210-250 g, traumatic shock induced by Noble-Collip drum trauma under anesthesia with sodium pentobarbital)[1]
Doses: 250 ng/kg/min
Route of Administration: Intravenous injection; continuous infusion; starting 15 minutes after trauma and continuing until the end of the experiment
Experimental Results: Mean survival time was extended to 2.6 hours. Inhibition of trauma-induced increase in plasma cathepsin D activity, reducing it from about 14 units/mg protein to about 9 units/mg protein. Reduction of plasma MDF activity, reducing it from about 58 units to about 30 units. In 7 out of 10 treated rats, mean arterial blood pressure increased to 108 mmHg in 0.5 hours and remained at that level for 2 hours.

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Animal/Disease Models:Sprague-Dawley mice (male, 210-250 g, sham surgery, non-invasive) [1]
Doses: 250 ng/kg/min
Route of Administration: Intravenous injection; continuous infusion; 5 hours
Experimental Results: 5 minutes after the start of infusion, mean arterial blood pressure decreased by 15 mmHg and increased by 10 mmHg after 15 minutes. After 5 hours, mean arterial blood pressure remained at 117 mmHg, lower than the initial 140 mmHg. No significant changes in heart rate were observed.

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Animal/Disease Models:Domestic cats (adults, sex not limited, 1.9 to 4.3 kg) [2]
Doses: 1 μg/min
Route of Administration: Enteral; infusion
Experimental Results: Mesenteric artery perfusion pressure decreased from 105 mmHg in the control group to 76 mmHg at 1 minute, 73 mmHg at 3 minutes, 72 mmHg at 5 minutes, 77 mmHg at 10 minutes and 76 mmHg at 30 minutes. Perfusion pressure returned to baseline (105 mmHg) 30 minutes after infusion was stopped. During infusion, all tested doses of norepinephrine (0.3, 1, 3 μg/ia), all tested frequencies of sympathetic nerve stimulation (1, 3, 10 times/second), and all tested doses of angiotensin II (0.3, 1 μg/ia) reduced vasoconstriction. Thirty minutes after the infusion ended, all suppressed vasoconstrictive responses returned to control levels.

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Animal/Disease Models:Mongrel cats (male or female, 2.0-4.5 kg) [3]
Doses: 0.3 μg; 1.0 μg; 3.0 μg; 10.0 μg
Route of Administration: Intravenous injection; rapid injection
Experimental Results: Compared with the control group with increased tension from 5-HT, the results of this study showed a significant decrease in central airway resistance (RL) and a significant increase in dynamic lung compliance (Cdyn) and semi-static compliance (C'stat'). At a dose of 0.3 μg, RL decreased from 38 cm H2O/L/sec to 35 cm H2O/L/sec, Cdyn increased from 4.0 mL/cm H2O to 4.5 mL/cm H2O, and C'stat' increased from 3.2 mL/cm H2O to 3.5 mL/cm H2O, but did not cause a significant change in pulmonary artery pressure (PPA). At a dose of 1.0 μg, RL decreased from 38 cm H2O/L/sec to 32 cm H2O/L/sec, Cdyn increased from 4.4 mL/cm H2O to 4.9 mL/cm H2O, and C'stat' increased from 3.4 mL/cm H2O to 3.9 mL/cm H2O, but did not cause a significant change in PPA. At a dose of 3.0 μg, RL decreased from 34 cm H2O/L/sec to 27 cm H2O/L/sec, Cdyn increased from 4.4 mL/cm H2O to 5.2 mL/cm H2O, C'stat' increased from 3.5 mL/cm H2O to 4.5 mL/cm H2O, and PPA significantly decreased from 25 mmHg to 23 mmHg. At a dose of 10.0 μg, RL decreased from 32 cm H2O/L/sec to 22 cm H2O/L/sec (a 32% reduction in elevated muscle tone, equivalent to 50% recovery to the pre-5-HT control value), Cdyn increased from 5.3 mL/cm H2O to 6.2 mL/cm H2O, and C'stat' increased from 4.1 mL/cm H2O to 5.1 mL/cm H2O, but PPA remained unchanged. In reducing respiratory rate, it is 3-10 times more effective than PGI2; at lower doses, it is also more effective than PGI2 in increasing dynamic heart rate. The time to maximum response (tmax) is 30 to 42 seconds, significantly shorter than that of PGI2 at equivalent doses. The duration of response (t1/2) is 52 to 103 seconds, with no significant difference compared to PGI2. Airway and vascular responses are unchanged after prior treatment with meclofenamic acid sodium.

[1]. Protective action of 6-keto-prostaglandin E1 in traumatic shock. Prostaglandins Med. 1979;2(4):277-284.

[2]. Inhibition of vasoconstrictor responses by 6-keto-PGE1 in the feline mesenteric vascular bed. Prostaglandins. 1980;19(2):299-310.

[3]. Abstract!. Neth J Med. 2002;60(11):418.

67786-53-2

Colorless to light yellow liquid

6-keto-Prostaglandin E1

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.)