r form

Bay 65-1942 R form is the less active R-form of Bay 65-1942. Bay 65-1942 is a selective and ATP-competitive IKKβ inhibitor.

EMD638683 is a highly selective SGK1 inhibitor with IC50 of 3 μM. EMD638683 R-Form is the R-form of EMD638683.

BD-AcAc 2 (Ketone Ester) 是一种酮单酯，是口服营养酮的来源。小鼠口服 BD-AcAc 2 后可提高血浆 乙酰乙酸和β-羟基丁酸水平、血液钠离子、血糖水平和血肌酐水平。BD-AcAc 2 可以一定程度预防脓毒症小鼠的肌无力。BD-AcAc 2 显示出提高动物机体耐力和运动能力的潜力。BD-AcAc 2 还可用于研究糖尿病或帕金森病。

Fipexide 是对氯苯乙酸衍生物，是哌嗪化学类的精神活性药物，作为促智药物，有用于老年痴呆的研究潜力。它可降低了纹状体腺苷酸环化酶的活性，通过多巴胺能神经传递对认知表现出积极的作用。

Arformoterol Tartrate ((R,R)-Formoterol tartrate) 是一种长效 β2-肾上腺素能受体 (β2-AR) 激动剂，Kd=2.9 nM。它是一种 Formoterol 的 (R,R)-对映异构体，可用于慢性阻塞性肺疾病 (COPD) 的研究。

Pactimibe is a ACAT inhibitor. It has anti-atherosclerotic activity.

Pactimibe sulfate (CS-505) 是一种双重的 ACAT1/2 抑制剂，能够作用于 ACAT1 (IC50: 4.9 μM)、ACAT2 (IC50: 3.0 μM)。Pactimibe sulfate 对 ACAT 表现出抑制作用，在肝细胞中 IC50=2.0 μM，在巨噬细胞中 IC50=2.7 μM，在 THP-1 细胞中 IC50=4.7 μM。Pactimibe sulfate 能够非竞争性地抑制 oleoyl-CoA (Ki: 5.6 μM)，显著抑制胆固醇酯的形成 (IC50: 6.7 μM)。Pactimibe sulfate 能够降低血浆胆固醇的活性，具有抗动脉粥样硬化的潜力。

Minnelide is an effective therapy against pancreatic cancer. Minnelide Inhibits Androgen Dependent, Castration Resistant Prostate Cancer Growth by Decreasing Expression of Androgen Receptor Full Length and Splice Variants. Minnelide reduced tumor volume in multiple models of pancreatic cancer. Minnelide was a more effective drug against pancreatic cancer models. It effectively reduced tumor burden and tumor related morbidity in different unique but complementary mouse models. It reduced metastatic spread and increased survival in the different models as well.

Arformoterol Tartrate (Standard) 是 Arformoterol Tartrate 的标准品，适用于定量分析、质量控制及生化实验等相关研究。Arformoterol Tartrate ((R,R)-Formoterol tartrate) 是一种长效 β2-肾上腺素能受体 (β2-AR) 激动剂，Kd=2.9 nM。它是一种 Formoterol 的 (R,R)-对映异构体，可用于慢性阻塞性肺疾病 (COPD) 的研究。

(Rac)-Apremilast D5 is a deuterium-labeled version of the enantiomer (R)-Apremilast, also known as (R)-CC-10004, which itself is one specific form of Apremilast.

SAR405 R enantiomer 是一种 PIK3C3/Vps34 抑制剂，也是活性低于 SAR405 的对映体。

(R)-Pantetheine (Pantetheine) 是VB5(泛酸)的生物活性形式，在自然界中以各种形式的含 Pantetheine 配体 （PCL） 的形式存在。(R)-Pantetheine 可增加血小板细胞膜流动性，抑制血小板聚集。

(S,R,S)-AHPC-C5-COOH (VH032-C5-COOH) is a synthesized E3 ligase ligand-linker conjugate, contains the VH032 VHL-based ligand and a linker to form PROTACs. VH-032 is a selective and potent inhibitor of VHL/HIF-1α interaction with a Kd of 185 nM, has the potential for the study of anemia and ischemic diseases[1].

(R,S,S)-VH032-Me 是一种 E3 泛素连接酶的配体 (ligand for E3 ubiquitin ligase)，能够通过 linker 同靶蛋白配体结合，生成 dTAGV-1-NEG。PROTAC 可诱导促癌蛋白进行泛素化降解。

(S,R,S)-AHPC-Boc derivative 1 (Compound 80-9; VH032-Boc derivative 1) 是一种选择性地靶向MALT1的蛋白酶体降解物。它通过招募 E3 泛素连接酶 CRBN，与MALT1形成三元复合物，从而引导MALT1的泛素化和蛋白酶体降解。此化合物通过干扰CBM复合体抑制NF-κB信号通路，并在ABC-DLBCL细胞中展现出诱导凋亡的潜力，适合作为MALT1依赖性癌症研究的潜在工具，包括弥漫性大B细胞淋巴瘤 (DLBCL)。

β2AR agonist 2 (compound 8a) 是 β2-肾上腺素能受体 (β2AR) 的激动剂。这是一种包含4-至7-元杂环的饱和氮环状化合物，其手性结构为含有必要羟基的碳的-R形式，增强细胞葡萄糖摄取(GU)的活性，显著刺激骨骼肌细胞摄取葡萄糖。β2AR agonist 2 可用于二型糖尿病研究(T2D)。

(S,R,S)-AHPC-C7-aminedihydrochloride 是 (S,R,S)-AHPC-C7-胺的二盐酸盐形式。(S,R,S)-AHPC-C7-amine 是一种合成的 E3 连接酶配体-linker 偶联物，包含基于 VH032 的 VHL 配体和一个 linker。(S,R,S)-AHPC-C7-amine 可用于合成靶向 ERRα 的 PROTAC降解剂。

(S,R,S)-AHPC-Me-piperazine-acetyl-PIP-AcOH 是 E3 泛素酶 VH032 的 VHL 配体与 Linker 的结合体。其 Linker 可与靶蛋白配体（例如 BCR-ABL1）进一步结合，构成PROTAC分子。

Levomefolate magnesium is the magnesium salt of the metabolite of folic acid (Vitamin B9) and it is a predominant active form of folate found in foods and in the blood circulation, accounting for 98% of folates in human plasma. It is transported across th

(R)-nitro-Blebbistatin is a more stable form of (+)-blebbistatin , which is the inactive form of (-)-blebbistatin . Prolonged exposure to blue light (450-490 nm) results in degradation of blebbistatin to an inactive product via cytotoxic intermediates, which may be problematic for its use in fluorescent live cell imaging applications. The addition of a nitro group stabilizes the molecule to circumvent its degradation by prolonged blue light exposure. (R)-nitro-Blebbistatin has the same stereochemistry as the inactive (+)-blebbistatin enantiomer.

IKD-8344 is a macrocyclic dilactone originally isolated from an actinomycete species and has diverse biological activities, including anticancer, antimicrobial, and anthelmintic properties.1,2,3 It is cytotoxic to L5178Y murine leukemia cells (IC50 = 0.54 ng/ml).1 IKD-8344 inhibits growth of the mycelial form of C. albicans (MIC = 6.25 μg/ml) and potentiates the activity of polymyxin B against the multidrug-resistant pathogenic bacterium B. cenocepacia.2,3 It is active against T. spiralis in vitro and in vivo.1 |1. Minami, Y., Yoshida, K., Azuma, R., et al. Structure of a novel macrodiolide antibiotic IKD-8344. Tetrahedron Lett. 33(48), 7373-7376 (1992).|2. Hwang, E.I., Yun, B.S., Yeo, W.H., et al. Compound IKD-8344, a selective growth inhibitor against the mycelial form of Candida albicans, isolated from Streptomyces sp. A6792. J. Microbiol. Biotechnol. 15(4), 909-912 (2005).|3. Loutet, S.A., El-Halfawy, O.M., Jassem, A.N., et al. Identification of synergists that potentiate the action of polymyxin B against Burkholderia cenocepacia. Int. J. Antimicrob. Agents 46(4), 376-380 (2015).

Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid.[1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D1 is produced physiologically from the sequential oxygenation of DHA by 15- and 5-lipoxygenase.[1] 17(R)-RvD1 is an aspirin-triggered epimer of RvD1 that reduces human polymorphonuclear leukocyte (PMN) transendothelial migration, the earliest event in acute inflammation, with equipotency to RvD1 (EC50 = ~30 nM).[3] 17(R)-RvD1 exhibits a dose-dependent reduction in leukocyte infiltration in a mouse model of peritonitis with maximal inhibition of ~35% at a 100 ng dose.[3] In contrast to RvD1, the aspirin-triggered form resists rapid inactivation by eicosanoid oxidoreductases. Analytical and biological comparisons of synthetic 17(R)-RvD1 with endogenously derived 17(R)-RvD1 have confirmed its identity as matching the natural product.[4]

Olsalazine-13C6is intended for use as an internal standard for the quantification of olsalazine by GC- or LC-MS. Olsalazine is an orally bioavailable prodrug form of the anti-inflammatory agent 5-aminosalicylic acid that is cleaved by bacterial azo reductases in the gut to generate active 5-ASA.1In vitro, olsalazine increases ion transport in isolated rabbit distal ileum when applied to the luminal side (ED50= 0.3 mM) and stimulates fluid transport in rat jejunum when used at a concentration of 5 mM.2,3Olsalazine (150 mg/kg for 8 days) improves stool consistency and decreases occult and gross bleeding as well as myeloperoxidase (MPO) activity and leukotriene B4levels in colon tissue in a mouse model of acute colitis induced by dextran sulfate .4Olsalazine also inhibits bovine xanthine oxidasein vitro(IC50= 3.4 mg/L) and lowers serum uric acid levels in a mouse model of hyperuricemia induced by oxonic acid when administered at a dose of 20 mg/kg.5Formulations containing olsalazine have been used in the treatment of inflammatory bowel disease (IBD) and ulcerative colitis. 1.Nugent, S.G., Kumar, D., Rampton, D.S., et al.Intestinal luminal pH in inflammatory bowel disease: Possible determinants and implications for therapy with aminosalicylates and other drugsGut48(4)571-577(2001) 2.Pamukcu, R., Hanauer, S.B., and Chang, E.B.Effect of disodium azodisalicylate on electrolyte transport in rabbit ileum and colon in vitro. Comparison with sulfasalazine and 5-aminosalicylic acidGastroenterology95(4)975-981(1988) 3.Mohsen, A.Q.M., Mulvey, D., Priddle, J.D., et al.Effects of olsalazine in the jejunum of the ratGut28(3)346-352(1987) 4.Murthy, S., Murthy, N.S., Coppola, D., et al.The efficacy of BAY y 1015 in dextran sulfate model of mouse colitisInflamm. Res.46(6)224-233(1997) 5.Niu, Y., Li, H., Gao, L., et al.Old drug, new indication: Olsalazine sodium reduced serum uric acid levels in mice via inhibiting xanthine oxidoreductase activityJ. Pharmacol. Sci.135(3)114-120(2017)

Epoxide hydrolases convert the EETs into vicinal diols, with the concurrent loss of much of their biological activity. The 8(S),9(R)-EET isomer is metabolized by platelet COX to form 8(S),9(R),11(R)-THETA, a trihydroxy fatty acid which may act as a renal vasoconstrictor.