IC50: 5 nM (NHE3, human), 10 nM (NHE3, rat)[1]
Tenapanor exhibits human and rat NHE3 with IC50 values of 5 and 10 nM, respectively. Human intestinal transporters NHE1, NHE2, TGR5, ASBT, and Pit-1 and the sodium-dependent phosphate transporter NaPiIIb are not inhibited by tenapanor at concentrations up to 10 to 30 μM[1].

Tenapanor 对人和大鼠 NHE3 的 IC50 值分别为 5 和 10 nM。人肠道转运蛋白 NHE1、NHE2、TGR5、ASBT 和 Pit-1 以及钠依赖性磷酸盐转运蛋白 NaPiIIb 在浓度高达 10 至 30 μM 时不会被 tenapanor 抑制[1]。

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Tenapanor (1 μM) 在跨一系列顶端磷酸盐浓度 (1-30 mM) 的人十二指肠和回肠单层细胞培养模型中，显著降低了顶侧到底侧的磷酸盐通量，表明其抑制了被动的细胞旁路磷酸盐吸收。[1]
Tenapanor (1 μM) 增加了人十二指肠和回肠单层细胞培养模型中的跨上皮电阻 (TEER)，这与细胞旁路通透性降低一致。[1]
Tenapanor (1 μM) 降低了人十二指肠单层细胞模型中的底侧到顶侧的磷酸盐通量，与其对顶侧到底侧吸收的影响相当，证实了其对双向细胞旁路磷酸盐通透性的降低作用。[1]
在人回肠单层细胞模型中，Tenapanor 在管腔pH 6.0 至 8.0 的范围内均降低了磷酸盐吸收，且在pH 7.0 和 8.0 时的降低幅度大于pH 6.0时。[1]
在pH 8.0条件下于Ussing室中培养的人十二指肠单层细胞中，通过稀释电位和双离子电位测量，Tenapanor 增加了TEER并降低了细胞旁路对钠、氯和磷酸盐的通透性。[1]
在CRISPR/Cas9生成的NHE3敲除 (KO) 人回肠单层细胞中，Tenapanor (1 μM) 对磷酸盐吸收、顶端磷酸盐浓度或TEER没有影响，证实其作用完全是通过靶向抑制NHE3介导的。[1]
Tenapanor (1 μM) 在小鼠回肠单层细胞培养模型（该模型中吸收主要由主动转运蛋白NaPi2b介导）中不影响磷酸盐吸收。[1]
Tenapanor (1 μM) 处理30、60或120分钟后，未引起人回肠单层细胞中紧密连接蛋白（zona occludens-1, occludin, claudin 7, claudin 3）定位的明显变化。[1]
内吞作用抑制剂 (Pitstop 2 和 dynasore) 不能阻断Tenapanor 在回肠单层细胞中诱导的TEER增加。[1]
在人回肠单层细胞中，其他降低细胞内pH的化合物（nigericin, BAM15, FCCP）也能增加TEER，效果与Tenapanor相似。[1]

在大鼠中，tenapanor（0.15、0.5 mg/kg；口服）可减少被动细胞旁磷酸盐的吸收[1]。当给予 tenapanor（0.15 mg/kg；口服；每天两次，持续 11 天）时，大鼠尿液中磷排泄的减少进一步减少 [2]。

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在大鼠肠道（空肠）环模型中，Tenapanor (10 μM) 将放射性磷酸盐吸收降低到与无钠条件下观察到的相似水平。[1]
在大鼠中，口服Tenapanor (0.5 mg/kg) 后，再给予不同浓度 (0.15-1.5 M) 的磷酸盐口服推注，能降低尿磷酸盐排泄，表明其抑制了肠道磷酸盐吸收。[1]
在喂食不同磷酸盐含量饲料的大鼠中，慢性给予Tenapanor (0.5 mg/kg，连续4天) 降低了尿磷酸盐排泄，表明其抑制了肠道磷酸盐吸收的一个恒定部分。[1]
在大鼠肠道内容物积聚研究中，Tenapanor (0.15 mg/kg) 在高磷酸盐餐后降低了尿磷酸盐和钠的排泄，并增加了钠和磷酸盐向盲肠的输送量（质量）和浓度，证实了小肠吸收减少。Tenapanor 增加了管腔水体积和钠浓度，但对盲肠钾、钙或镁的浓度没有显著影响。盲肠氯浓度适度增加。[1]
在健康大鼠中给予Tenapanor (0.5 mg/kg) 14天，尿钠和磷酸盐排泄减少，而尿氯和钾排泄不受影响。血浆钠和磷酸盐浓度不变。磷酸盐和钠的肾脏清除率降低。在常规磷酸盐饮食的健康大鼠中，Tenapanor 对磷酸盐调节激素（FGF-23、甲状旁腺激素、维生素D）的影响极小。[1]
给予Tenapanor 14天的大鼠RNA-seq分析显示，空肠、回肠和近端结肠的NHE3 mRNA表达增加，远端结肠的上皮钠通道γ亚基 (ENaCγ) 表达增加。氯转运蛋白/交换蛋白 (SLC26A3, SLC26A6, CFTR) 的表达没有变化。[1]
在大鼠中，Tenapanor (0.5 mg/kg，14天) 适度但显著降低了远端空肠和回肠中NaPi2b mRNA的表达（减少约30%）。免疫组化证实空肠中NaPi2b蛋白染色强度适度降低。[1]
从Tenapanor处理的大鼠十二指肠和空肠分离的刷状缘膜囊泡 (BBMV) 显示，对钠依赖性磷酸盐摄取或钠依赖性葡萄糖吸收影响很小。[1]
在小鼠体内回肠环模型中，Tenapanor (10 μM) 在野生型和NaPi2b敲除小鼠中均引起小幅、不显著的磷酸盐吸收减少。[1]
在大鼠中，Tenapanor (0.5 和 10 mg/kg) 抑制了放射性磷酸盐的吸收，但不影响放射性甘露醇（一种细胞旁路大分子吸收标志物）的吸收。[1]
在大鼠中，Tenapanor (0.15 mg/kg) 不影响标准化餐后小肠对膳食葡萄糖的吸收。[1]
在健康志愿者的1期研究中，Tenapanor (15 mg，每日两次，连续4天) 显著增加了日均粪便磷排泄，并显著降低了日均尿磷和尿钠排泄。尿钾排泄不受影响。[1]

通过测量Tenapanor抑制顶端酸分泌来评估其对NHE3的效力，实验使用人和小鼠回肠单层细胞培养模型。由NHE3介导的质子分泌耦合钠吸收引起的顶端培养基酸化，通过pH敏感酚红的颜色变化进行监测，或使用荧光pH指示剂染料BCECF-AM进行定量测定。定量测定中，荧光发射比率（激发光440 nm/490 nm，发射光535 nm）的降低反映pH降低。进行浓度-效应研究以确定IC50值。[1]
在酸负荷后，通过测量Tenapanor对NHE3介导的细胞内pH (pHi) 恢复的影响来评估其活性，实验使用人十二指肠和回肠单层细胞培养模型。用pH敏感染料BCECF-AM负载细胞。通过在无钠培养基中孵育诱导细胞内酸化。通过在存在或不存在Tenapanor的情况下，添加不同管腔pH水平（例如6.0, 7.0）的含钠培养基来启动恢复。反映NHE3活性的pHi恢复速率通过荧光法监测。[1]

Tenapanor抑制肠上皮细胞模型中的细胞旁磷酸盐通量。
来自人类或小鼠胃肠道活检的肠上皮干细胞作为单层培养，可以监测穿过肠上皮的离子转运。类肠单层包含肠上皮细胞谱系的多样性，模拟每个单独肠段的特定基因表达模式，以段特异性的方式表达适当的内源性离子转运蛋白（例如NHE3和NaPi2b），极化形成紧密连接，与claudin和其他紧密连接蛋白的段特异性表达形成紧密连接并产生体内观察到的预期负管腔电位。因此，分化的类肠单层能够研究跨细胞和细胞旁的磷酸盐吸收[1]。

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肠上皮干细胞单层培养模型[1]。
按照Kozuka等人的详细描述，在Transwell上培养和分化肠上皮干细胞单层。根据哥白尼集团机构审查委员会批准的方案，从男性供体的可见健康组织中获得干细胞来源的人类活检组织。通过用新鲜补充的基础培养基和无磷酸盐的Dulbecco改良Eagle培养基洗涤顶端和基底外侧两次，在每个分化的单层培养中很好地开始实验。如文中所述，化合物仅在单层的顶端侧给药；使用等浓度的DMSO作为对照。磷酸盐浓度和pH值如文中所述进行操作。

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人和小鼠肠道上皮干细胞来源的肠类器官单层细胞在Transwell插入式培养皿上培养和分化。这些单层细胞模拟肠道离子转运生理，以节段特异性方式表达内源性转运蛋白（NHE3, NaPi2b），形成紧密连接，并产生管腔负性电位。[1]
对于磷酸盐通量实验，清洗单层细胞，并在顶端和基底外侧室中加入含有确定磷酸盐浓度的培养基。将Tenapanor或载体添加到顶端侧。孵育（例如4小时或过夜）后，通过离子色谱法测量顶端和基底外侧培养基中的磷酸盐浓度。计算磷酸盐通量。使用电压/电阻计测量跨上皮电阻 (TEER)。[1]
为了评估细胞旁路离子通透性，将人十二指肠单层细胞或小鼠空肠条固定在Ussing室中。在短路条件下测量氯化钠稀释电位和磷酸盐双离子电位，以计算细胞旁路对钠 (pNa+)、氯 (pCl-) 和磷酸盐 (pPO43-) 的通透性。将Tenapanor或载体添加到黏膜侧。[1]
使用pH敏感荧光染料BCECF-AM测量细胞内pH (pHi)。细胞负载染料，用双激发光（440 nm和490 nm）和535 nm发射光测量荧光。荧光比率（490/440）取决于pH。在改变顶端培养基pH或添加Tenapanor等操作后监测pHi的变化。[1]
使用CRISPR/Cas9介导的基因编辑技术生成NHE3敲除人回肠上皮干细胞克隆。通过DNA测序、NHE3蛋白的Western印迹和功能测定（缺乏顶端培养基酸化、酸负荷后无pHi恢复）确认敲除。这些敲除单层细胞用于测试Tenapanor作用的特异性。[1]
通过用网格蛋白介导的内吞作用抑制剂 (Pitstop 2) 或动力蛋白抑制剂 (dynasore) 预处理回肠单层细胞，研究了内吞作用在Tenapanor诱导的TEER增加中的作用。通过它们阻止卡巴胆碱诱导的NHE3内化的能力确认了这些抑制剂的有效性。然后在添加Tenapanor后测量TEER。[1]
测试了其他细胞内酸化剂对TEER的影响。用离子载体尼日利亚菌素或线粒体解偶联剂 (BAM15, FCCP) 处理回肠单层细胞，这些物质能降低pHi。测量TEER并与对照组比较。[1]
通过免疫细胞化学评估了用Tenapanor或载体处理30、60和120分钟的人回肠单层细胞中紧密连接蛋白（zona occludens-1, occludin, claudin 7, claudin 3）的定位。[1]
在磷酸盐吸收主要为跨细胞且由NaPi2b介导的小鼠回肠单层细胞模型中，测试了NaPi2b抑制剂 (NTX-9066) 的效果。将单层细胞与抑制剂、Tenapanor或载体孵育不同时间（4小时、2天、3天），并测量顶端磷酸盐浓度。[1]

Animal/Disease Models: Rats (intestinal loop model)[1]
Doses: 0.15, 0.5 mg/kg
Route of Administration: Po
Experimental Results: decreased passive paracellular phosphate absorption by decreased urinary phosphate and sodium excretion after the high-phosphate meal and increased sodium and phosphate delivery to the cecum.

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Animal/Disease Models: 8 weeks, 250 g male Sprague–Dawley rats[2]
Doses: 0.15 mg/kg in combination with sevelamer (0%, 0.75%, 1.5%, and 3% (wt/wt))
Route of Administration: po (oral gavage); twice-daily for 11 days
Experimental Results: Dramatically augmented the reduction in urinary phosphorus excretion.

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Rat intestinal loop model: Rats were anesthetized. A segment of jejunum was isolated, and the lumen was rinsed. A buffer containing radioactive phosphate (33P) with or without tenapanor (10 μM) or with sodium-free buffer was injected into the loop. The loop was returned to the abdomen for a specified time. Phosphate absorption was determined by measuring the disappearance of radioactivity from the loop and/or its appearance in plasma. [1]
Oral phosphate bolus and urinary excretion in rats: Rats were pretreated with tenapanor (0.5 mg/kg) or vehicle by oral gavage. Subsequently, an oral bolus of phosphate solution at varying concentrations (0.15-1.5 M) was administered. Urine was collected for 4 hours, and phosphate excretion was measured. [1]
Chronic dietary phosphate study in rats: Rats were fed diets with different phosphate contents. After baseline urine collection, rats were treated with tenapanor (0.5 mg/kg) or vehicle orally twice daily for 4 days. Urine was collected during treatment for phosphate excretion analysis. [1]
Enteropooling study in rats: Rats were trained to consume a standardized high-phosphate (1.2%) meal within a short period. On the study day, rats were treated with tenapanor (0.15 mg/kg) or vehicle before the meal. At defined time points after meal initiation, rats were euthanized, and the cecum was removed. Cecal contents were weighed, and the concentrations of ions (sodium, phosphate, potassium, chloride, calcium, magnesium) were measured by ion chromatography. Urine was also collected for ion excretion analysis. [1]
14-day repeat dose study in rats: Healthy rats were dosed orally with tenapanor (0.5 mg/kg) or vehicle twice daily for 14 days. Urine was collected over 24-hour periods at various time points for measurement of sodium, phosphate, chloride, and potassium excretion. Blood was collected at the end for plasma ion and hormone (FGF-23, PTH, vitamin D) analysis. Renal clearance was calculated. Gastrointestinal tissues were collected for RNA-seq analysis and NaPi2b mRNA expression measurement by qPCR. [1]
NaPi2b expression and BBMV study in rats: In a separate study, rats were treated with tenapanor or vehicle for a period. Jejunum tissue was collected for immunohistochemistry staining of NaPi2b protein. For BBMV preparation, duodenum and jejunum were collected from treated rats. BBMVs were isolated by a Mg2+ precipitation method. Uptake of radioactive phosphate or glucose into BBMVs was measured in the presence or absence of sodium. [1]
Mouse ileum loop model: Wild-type and NaPi2b knockout mice were used. Under anesthesia, an ileal loop was prepared and injected with a buffer containing radioactive phosphate and tenapanor (10 μM) or vehicle. Phosphate absorption was determined after a set incubation period. [1]
Mannitol and glucose absorption studies in rats: For mannitol absorption, rats received an oral dose of tenapanor (0.5 or 10 mg/kg) or vehicle, followed by an oral dose containing 3H-mannitol and 33P-phosphate. Blood was sampled over time to measure radioactivity. For glucose absorption, rats pretreated with tenapanor (0.15 mg/kg) or vehicle consumed a standardized meal over 4 hours. At specified times, rats were euthanized, and the entire small intestine was removed. Luminal glucose content was measured. [1]

Absorption, Distribution and Excretion
Tenapanor undergoes very minimal systemic absorption following oral administration. During clinical trials, plasma concentrations were below the limit of quantitation (i.e. less than 0.5 ng/mL) in the majority of samples from healthy subjects - for this reason, typical pharmacokinetic values related to absorption such as AUC and Cmax were unable to be ascertained. The effects of tenapanor are greatest when administered 5 to 10 minutes before meals.
Following administration of a radio labeled dose of tenapanor, 70% of the radioactivity was excreted in the feces within 120 hours of administration and 79% within 240 hours. Approximately 65% of the total dose is excreted as unchanged parent drug within 144 hours of administration. Only 9% of the administered dose was found in the urine, existing primarily as metabolites. Tenapanor's M1 metabolite is excreted unchanged in the urine and accounts for approximately 1.5% of the total dose within 144 hours of administration.

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Metabolism / Metabolites
The majority of tenapanor's metabolism to its primary metabolite, M1, is catalyzed via CYP3A4/5. Exposure of tenapanor to hepatic CYP enzymes is likely limited due to its minimal systemic absorption, so its metabolism may be due to intestinal CYP enzyme activity. The M1 metabolite of tenapanor is a P-glycoprotein substrate and, in contrast to its parent drug, can be detected in plasma, reaching a C_max of approximately 15 ng/mL at steady state. It is not considered active against NHE3.

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Biological Half-Life
Tenapanor's FDA label states that its half-life could not be determined during clinical trials due to its minimal systemic absorption resulting in plasma concentrations below the limit of quantitation (i.e. less than 0.5 ng/mL).

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Tenapanor is described as a "minimally absorbed" small-molecule inhibitor that acts locally in the gastrointestinal tract. [1]
In healthy human volunteers, systemic drug exposure was reported to be minimal. [1]

Hepatotoxicity
When given orally, tenapanor has minimal systemic absorption and has not been associated with elevations in serum enzymes or bilirubin or with instances of clinically apparent liver injury. Since approval and general availability of tenapanor, there have been no published reports of liver injury attributed to its use.
Likelihood score: E (unlikely cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Tenapanor is essentially non-absorbed systemically, with undetectable plasma concentrations following oral administration. The minimal systemic absorption of tenapanor will not result in a clinically relevant exposure to breastfed infants. No special precautions are necessary.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Both tenapanor and its principle metabolite, M1, are highly plasma protein bound at approximately 99% and 97%, respectively. The specific proteins to which tenapanor and its metabolite binds have yet to be elucidated.

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The study mentions that in healthy volunteers, treatment with tenapanor did not affect serum bicarbonate or urinary pH, suggesting no perturbation of systemic acid-base balance. [1]

[1]. Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability. Sci Transl Med. 2018 Aug 29;10(456):eaam6474.

[2]. Combination treatment with tenapanor and sevelamer synergistically reduces urinary phosphorus excretion in rats. Am J Physiol Renal Physiol. 2021 Jan 1;320(1):F133-F144.

Tenapanor is a novel, small molecule medication approved in September 2019 for the treatment of constipation-predominant irritable bowel-syndrome (IBS-C). It was first designed and synthesized in 2012. As an inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3) transporter, it is the first and currently only medication within its class and therefore exists as a novel alternative in the treatment of IBS-C. In October 2023, tenapanor was approved for the treatment of chronic kidney disease.
Tenapanor is a Sodium-Hydrogen Exchanger 3 Inhibitor. The mechanism of action of tenapanor is as a Sodium-Hydrogen Exchanger 3 Inhibitor, and Organic Anion Transporting Polypeptide 2B1 Inhibitor.
Tenapanor is a small molecular inhibitor of the sodium/hydrogen ion exchanger-3 (NHE3) used to treat constipation predominant irritable bowel syndrome (IBS). Tenapanor has minimal systemic absorption and has not been associated with serum enzyme elevation during therapy nor has it been linked to cases of clinically apparent liver injury.
See also: Tenapanor Hydrochloride (active moiety of).

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Drug Indication
Tenapanor is indicated for the treatment of constipation-predominant irritable bowel syndrome (IBS-C) in adults. It is also indicated to reduce serum phosphorus in adults with chronic kidney disease (CKD) on dialysis as add-on therapy in patients who have an inadequate response to phosphate binders or who are intolerant of any dose of phosphate binder therapy.

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Mechanism of Action
Tenapanor is a locally-acting small molecule inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3), an antiporter expressed on the apical surface of enterocytes in the small intestine and colon which is involved in sodium-fluid homeostasis. By inhibiting this antiporter tenapanor causes retention of sodium within the lumen of the intestine - this results in an osmotic gradient that draws water into the lumen and softens stool consistency. There is some evidence that tenapanor can inhibit the uptake of dietary phosphorus in the gastrointestinal tract, though the exact mechanism of this activity has yet to be elucidated.

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Pharmacodynamics
Through the inhibition of dietary sodium absorption tenapanor causes an increase in water secretion into the intestines, thereby decreasing transit time and softening stool consistency.

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Tenapanor is an investigational drug for the treatment of hyperphosphatemia in patients with chronic kidney disease (CKD), particularly end-stage renal disease (ESRD) on dialysis. [1]
Its primary mechanism of action is local inhibition of the sodium/hydrogen exchanger 3 (NHE3) in the gastrointestinal tract. This inhibition leads to intracellular acidification in enterocytes, which modulates tight junctions, increases transepithelial electrical resistance (TEER), and specifically reduces the paracellular permeability to phosphate. This reduces the passive paracellular absorption of dietary phosphate, which is quantitatively the major route of phosphate absorption at typical luminal concentrations. [1]
Tenapanor also modestly decreases the expression of the active intestinal phosphate transporter NaPi2b, preventing compensatory increases in transcellular phosphate uptake. It does not directly inhibit NaPi2b activity. [1]
The effect of tenapanor on ion absorption appears specific to sodium and phosphate. It does not significantly affect the absorption of potassium, calcium, magnesium, chloride (overall balance), glucose, or macromolecules like mannitol under physiological conditions. [1]
Tenapanor retains its ability to inhibit phosphate absorption even at high luminal phosphate concentrations, unlike phosphate binders. This may allow for a less restricted diet in patients. [1]
Clinical studies cited in the literature indicate that tenapanor significantly reduces serum phosphate and fibroblast growth factor 23 (FGF-23) in ESRD patients with hyperphosphatemia receiving dialysis. [1]
A limitation noted in the study is that the molecular identity of the paracellular phosphate pore affected by tenapanor remains unknown. [1]

C50H66CL4N8O10S2

1145.0486

1142.309

C, 52.45; H, 5.81; Cl, 12.38; N, 9.79; O, 13.97; S, 5.60

1234423-95-0

Tenapanor hydrochloride;1234365-97-9

71587953

Typically exists as white to off-white solids at room temperature

1.3±0.1 g/cm3

1.590

4.85

235Ų

6

14

29

74

1770

2

ClC1=C([H])C(=C([H])C2=C1C([H])([H])N(C([H])([H])[H])C([H])([H])[C@@]2([H])C1C([H])=C([H])C([H])=C(C=1[H])S(N([H])C([H])([H])C([H])([H])OC([H])([H])C([H])([H])OC([H])([H])C([H])([H])N([H])C(N([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])N([H])C(N([H])C([H])([H])C([H])([H])OC([H])([H])C([H])([H])OC([H])([H])C([H])([H])N([H])S(C1=C([H])C([H])=C([H])C(=C1[H])[C@@]1([H])C2C([H])=C(C([H])=C(C=2C([H])([H])N(C([H])([H])[H])C1([H])[H])Cl)Cl)(=O)=O)=O)=O)(=O)=O)Cl

DNHPDWGIXIMXSA-CXNSMIOJSA-N

InChI=1S/C50H66Cl4N8O10S2/c1-61-31-43(41-27-37(51)29-47(53)45(41)33-61)35-7-5-9-39(25-35)73(65,66)59-15-19-71-23-21-69-17-13-57-49(63)55-11-3-4-12-56-50(64)58-14-18-70-22-24-72-20-16-60-74(67,68)40-10-6-8-36(26-40)44-32-62(2)34-46-42(44)28-38(52)30-48(46)54/h5-10,25-30,43-44,59-60H,3-4,11-24,31-34H2,1-2H3,(H2,55,57,63)(H2,56,58,64)/t43-,44-/m0/s1

3-((S)-6,8-dichloro-2-methyl-1,2,3,4-tetrahydroisoquinolin-4-yl)-N-(26-((3-((S)-6,8-dichloro-2-methyl-1,2,3,4-tetrahydroisoquinolin-4-yl)phenyl)sulfonamido)-10,17-dioxo-3,6,21,24-tetraoxa-9,11,16,18-tetraazahexacosyl)benzenesulfonamide

RDX 5791; AZD 1722; RDX-5791; AZD1722; RDX5791; AZD-1722; Tenapanor free base;Tenapanor; 1234423-95-0; KHK7791; KHK-7791;

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)

DMSO : ~50 mg/mL (~43.67 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (2.18 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: 2.5 mg/mL (2.18 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (2.18 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 2.5 mg/mL (2.18 mM) in 5% DMSO + 95% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。