pge1

Prostaglandin E1 (Alprostadil) 是一种前列腺素受体配体，对小鼠 EP1、EP2、EP3、EP4和 IP 的 Ki 值分别为 36、10、1.1、2.1 和 33 nM。它诱导血管舒张并抑制血小板聚集，可作为血管扩张剂用于外周血管疾病的研究。

Limaprost (17α,20-dimethyl-δ2-PGE1) 是PGE1类似物，也是口服具有活性的血管舒张剂。它能够增加血流量以及减少血小板聚集。它具有抗心绞痛的功能，可用于疼痛的缓解，以及用于研究缺血性症状。

15-epi-PGE1 (15R-Prostaglandin E1; 15-Epiprostaglandin E1) 作为PGE1的立体异构体，在生物活性方面显得较为低下。该化合物为人胎盘15-羟基前列腺素脱氢酶 (15-PGDH) 的非竞争性抑制剂，具有170 μM的IC50值。

Alprostadil sodium 是一种前列腺素受体配体，对小鼠 EP1、EP2、EP3、EP4和 IP 的 Ki 值分别为 36、10、1.1、2.1 和 33 nM。它诱导血管舒张并抑制血小板聚集，可作为血管扩张剂用于外周血管疾病的研究。

Alprostadil ethyl ester is a biochemical used in the treatment of scleroderma.

13,14-dihydro-15(R)-Prostaglandin E1 (13,14-dihydro-15(R)-PGE1)为13,14-二氢-PGE1的同分异构体，特点在于其C-15位的羟基呈R构型，非自然形态。

Prostaglandin E1 (PGE1), though not predominantly found in nature, plays a significant role in clinical treatments, addressing conditions such as peripheral occlusive vascular disease, erectile dysfunction, and neonatal cardiology issues. The metabolism of PGE1 primarily begins with the oxidation at C-15, producing 13,14-dihydro-15-keto PGE1 as its major metabolite. Alternatively, inhibiting this pathway or overwhelming it with too much PGE1 could potentially enhance the production of 2,3-dinor metabolites, like 2,3-dinor PGE1, though their biological activities remain unreported. Cayman Chemical stands out as a prominent provider of prostaglandins and their metabolites, uniquely manufacturing 2,3-dinor PGE1.

Tetranor-Prostaglandin E1 (tetranor-PGE1), a metabolite of PGE1 and PGE2, undergoes formation through β-oxidation.

SC 31391 is a PGE1 analog.

13,14-dihydro-15-keto Prostaglandin E1 可抑制 ADP 诱导的人离体富血小板血浆中的血小板聚集（IC50=14.8 μg mL），也是 PGE1 代谢物。

15(S)-15-methyl PGE2 is a potent, metabolically stable analog of PGE2. It is a potent gastric antisecretory and antiulcer compound. 15(S)-15-methyl PGE2 binds to human myometrium with twice the affinity of PGE2 and is ten times more potent than PGE1 in contracting uterine smooth muscle.

8-iso Prostaglandin A1 (8-iso PGA1) is an isoprostane and a member in a large family of prostanoids of non-cyclooxygenase origin. It occurs as a common minor impurity in most commercial preparations of PGE1. The biological activity of 8-iso PGA1 has not been studied in depth or reported in the literature.

8-iso Prostaglandin F2β (8-iso PGF2β) is an isomer of PGF2α of non-enzymatic origin. It is one of 64 possible isomers of PGF2α which can be produced by free radical peroxidation of arachidonic acid. 8-iso PGF2β exhibits very weak contraction of human umbilical vein artery and does not promote aggregation of human whole blood. However, 8-iso PGF2β moderately contracts both the canine and porcine pulmonary vein, although the effect is much weaker than that exhibited by other isoprostanes such as 8-iso PGE1, 8-iso PGE2, or 8-iso PGF2α. 8-iso-15-keto PGF2β is a potential metabolite of 8-iso PGF2β via the 15-hydroxy PG dehydrogenase pathway. There are no published reports on the formation or biological activity of 8-iso-15-keto PGF2β.

Prostaglandin A1 (PGA1) was first isolated as a dehydration product of the PGE1 compounds found in human semen. 15-keto PGA1 is a metabolite of PGA1, produced by 15-hydroxy PG dehydrogenase. It can be produced from PGA1 in pig lung, trachea, aorta, and pulmonary artery tissue preparations. 15-keto PGA1, given at a concentration of 6 μM, causes vasoconstriction of rabbit lung that is comparable to that induced by angiotensin II.

16,16-dimethyl Prostaglandin E1 是 PGE1 (T1626) 类似物，可诱导支气管收缩和血管平滑肌收缩，并抑制吲哚美辛诱导的细胞伸长。

6-keto Prostaglandin E1 是 PGE1 的生物活性衍生物，在抗血小板聚集和解聚作用方面发挥作用。

13,14-dihydro Prostaglandin E1 (13,14-dihydro PGE1) is a biologically active metabolite of PGE1 with comparable potency to the parent compound. It is an inhibitor of ADP-induced platelet aggregation in human PRP and washed platelets with IC50 values of 31 and 21 nM, respectively. 13,14-dihydro PGE1 is a slightly more potent inhibitor of ADP-induced human platelet aggregation than PGE1 which has an IC50 value of 40 nM. Also, 13,14-dihydro PGE1 was shown to activate adenylate cyclase in NCB-20 hybrid cells with a Kact value of 668 nM.

8,11,14-Eicosatrienoic acid, also known as dihomo-γ-linolenic acid , is a polyunsaturated fatty acid (PUFA) produced from γ-linolenic acid by the action of fatty acid elongases. It can be metabolized by the cyclooxygenase pathway to produce 1-series prostaglandins (PGs) (e.g., PGE1). (±)14(15)-EpEDE is an EpEDE acid formed from 8,11,14-eicosatrienoic acid. This monoepoxide can be generated from the PUFA, in vitro, by the action of a strong oxidizing agent. Alternatively, this compound may be produced, in vivo, by epoxidation of the PUFA by cytochrome P450 epoxygenases. The biological properties of this compound are poorly understood.

The prostaglandin E receptor 4 (EP4) is one of four G protein-coupled receptors that mediate the actions of prostaglandin E2 . Binding of PGE2 to the EP4 receptor causes an increase in intracellular cyclic AMP, which plays important roles in bone formation and resorption, cancer, and atherosclerosis. KMN-80 is a substituted γ-lactam (pyrrolidinone) derivative of PGE1 that acts as a selective and potent agonist of EP4 with an IC50 value of 3 nM (IC50 = 1.4 μM for EP3 and > 10 μM for all other prostanoid receptors). In functional assays it has been shown to stimulate secreted alkaline phosphatase gene reporter activity in EP4-transfected HEK293 cells with an EC50 value of 0.19 nM, demonstrating >5,000 and 50,000-fold selectivity against EP2 and TP, respectively. KMN-80 can induce the differentiation of bone marrow stem cells from both young and aged rats into osteoblasts in vitro (EC50s = 20 and 153 nM, respectively) and exhibits favorable tolerability up to at least 10 μM, whereas the EP4 agonist L-902,688 is highly cytotoxic at similar concentrations in these cells. KMN-80 has been used to repair calvarial defects in an in vivo rat craniomaxillofacial reconstruction model (rate of reduction in defect size equivalent to BMP-2 treated rats) and to promote bone formation in a rat incisor tooth socket model.

tetranor-PGEM is the major urinary metabolite of PGE1 and PGE2, and is used as a marker of PGE2 biosynthesis.[1],[2] About 15% of an infused dose of PGE2 appears as this metabolite in the urine of humans. Normal healthy males excrete 7-40 μg of tetranor-PGEM over a 24-hour period.[1]

MRS2395 是一种二戊酰衍生物，是一种 P2Y12 受体的有效拮抗剂。MRS2395 抑制 ADP 诱导的血小板活化 (Ki: 3.6 μM)。MRS2395 在 PGE1 存在下，对大鼠血小板中 ADP 诱导的 cAMP 具有抑制作用 (IC50: 7 μM)。MRS2395 增强血小板致密颗粒释放以响应 TRAP-6。

BMY-42393 is orally active and selective platelet aggregation inhibitor. BMY-42393 is also a prostacyclin partial agonist that inhibited ADP, collagen and thrombin-induced platelet aggregation (IC50 range 0.3 - 2.0 microM). BMY-42393 stimulated platelet adenylate cyclase activity (EC50 = 25 nM). Platelets treated with BMY 42393 showed an elevation of cAMP levels and activation of cAMP-dependent protein kinase. BMY 42393 also inhibited thrombin-induced elevation of intracellular free calcium. BMY 42393 competed for radiolabeled iloprost and PGE1 binding to platelet membranes (IC50; 170 nM and 130 nM, respectively).

SC 34301 (Enisoprost)为有效的口服活性PGE1类似物，显著降低细菌移位并提升烧伤小鼠存活率。

Rp-Adenosine-5'-O-(1-thiotriphosphate)（Rp-ATP-α-S）是一种含硫核苷酸衍生物ATP-α-S的异构体，同时也是嘌呤P2Y1受体的激动剂。在表达人类P2Y1受体的HEK293细胞中，Rp-ATP-α-S能增加钙的动员（EC50 = 75 nM）。该化合物与洗涤的人类孤立血小板结合（Ki = 156 nM），抑制由ADP引发的人类富血小板血浆（PRP）的聚集（pA2 = 4.74），并且能够抑制前列腺素E1（PGE1）在人类孤立PRP中引发的cAMP产生（pA2 = 5.26）。同时，Rp-ATP-α-S还能引起用氨基甲酰胆碱预先缩紧的豚鼠结肠条带的松弛（EC50 = 56 nM）。此外，Rp-ATP-α-S已经被用于合成被细菌核糖开关识别的环状二核苷酸。