at-iii

H-D-Phe-Pip-Arg-pNA dihydrochloride (S-2238 dihydrochloride )是一种显色底物，模仿了纤维蛋白原Aα链N端片段，即凝血酶的天然底物。H-D-Phe-Pip-Arg-pNA dihydrochloride 专为凝血酶检测而设计，用于抗凝血酶-肝素辅因子(AT-III)的定量。利用该底物的AT-III检测方法以其灵敏度、准确性和实施的便捷性而特别闻名。

PF-04859989 HCl 是不可逆的犬尿氨酸转氨酶 KAT II 抑制剂，可透过血脑屏障，抑制 hKATⅡ 和 rKATⅡ 的 IC50分别为 23 和 263 nM。它对 KATⅡ 的选择性高于人 KATⅠ、KATⅢ 和 KATⅣ (IC50分别为22、11和 >50 μM)。

Bisdemethoxycurcumin (Curcumin III) 是一种具有抗炎及抗氧化作用的姜黄素。

Beauveriolide III 是一种存在于 Beauveria 属真菌中的环肽类化合物，可抑制脂滴形成（3-10 μM 时）及胆固醇合成（IC50=0.41 μM）。该化合物还能抑制酰基辅酶 A:胆固醇酰基转移酶（ACAT）活性（IC50=5.5 μM），并在 Ldlr-/- 和 ApoE-/- 小鼠模型中减少动脉粥样硬化斑块大小（25-50 mg/kg）。

VU0155094 (ML 397) 是一种正变构调节剂，对各种 III 组 mGluR 具有不同的活性

ARQ 069 (3.8-60 μM; for 2 hours) reduces the degree of phosphorylation of FGFR (predominantly FGFR2) in a concentration-dependent manner, without decreasing β-actin. ARQ 069 shows an affinity for FGFR2 of 5.2 μM. ARQ 069 inhibits FGFR phosphorylation in K

PD-1/PD-L1-IN-51 (Compound III-4) 作为一种有效的PD-1/PD-L1抑制剂，其IC50值针对hPD-L1为2.9 nM。通过直接结合至PD-L1，该化合物阻碍了PD-1与PD-L1之间的交互作用，并促进了IFN-γ的释放，显示出对肿瘤的抑制能力。

UNBS3157是一种新型的非血液毒性萘酰亚胺衍生物，具有强大的抗肿瘤活性，能够通过DNA插入作用和毒化拓扑异构酶IIalpha来与DNA结合。与之相关的萘酰亚胺类化合物Amonafide在二期乳腺癌试验中表现出了活性，但由于限制剂量的骨髓毒性，目前尚未进入三期临床试验。相比之下，UNBS3157的最大耐受剂量比Amonafide高出3-4倍，并且在显示出显著抗肿瘤效果的剂量下未引起小鼠的血液毒性。此外，在活体内模型中，包括(i) L1210鼠白血病、(ii) MXT-HI鼠乳腺腺癌、以及(iii)人类A549非小细胞肺癌和BxPC3胰腺癌原位模型中，UNBS3157显示出优于Amonafide的效果。

Plozasiran（此前称为 ARO-APOC3）是一种首创型在研 RNA 干扰（RNA interference，RNAi）治疗药物，其被特异性设计用于主动抑制肝脏中载脂蛋白 C-III（APOC3）的生成。APOC3 是甘油三酯富集脂蛋白（triglyceride-rich lipoproteins，TRLs）的关键结构与功能组成成分，也是全身甘油三酯代谢的核心调控因子。通过靶向性转录后基因沉默机制，Plozasiran 在基因表达层面干预脂质代谢异常，从而为血脂紊乱的治疗提供了一种精准且机制明确的治疗策略。

GSM III 是 γ-分泌酶复合物 (GSEC) 的调节剂。GSM III 在蛋白酶 (NCT、PSEN) 和底物 APPC99 之间的细胞外界面对淀粉样 β 蛋白 (Aβ) 的长度进行显著调节。GSM III 可用于阿尔茨海默病 (AD) 的研究。

Gonyautoxin III (GTX-III) 是一种麻痹性贝类毒素，能够在轴突水平阻断电压门控钠通道 (voltage-gated sodium channels)，其IC50值为14.9 nM，从而阻碍神经冲动的传导。Gonyautoxin III 对小鼠神经母细胞瘤细胞表现出杀伤活性，并可用于癌症和神经系统疾病的研究。

GSK 932121 is a potent antimalarial agent. GSK 932121 inhibits selectively the electron-transport chain in P. falciparum at the cytochrome bc1 level (complex III).

β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990). β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3 References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990).

Collismycin A is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities, including antibacterial, antiproliferative, and neuroprotective properties. It is active against a variety of bacteria (MICs = 6.25 and 100 μg/ml) and fungi (MICs = 12.5-100 μg/ml). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC50s = 0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC50 = 56.6 μM) but not MDA-MD-231 breast cancer cells (IC50 = >100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) at a 2:1 ratio, and the addition of iron ions inhibits the antiproliferative effect of collismycin A on HeLa cells, an effect that does not occur with the addition of zinc, manganese, copper, or magnesium ions. Collismycin A (1 μM) prevents apoptosis in the brain region of zebrafish larvae by 44% in a model of neuronal cell death induced by all-trans retinoic acid .

CAY10721 is an inhibitor of sirtuin 3 (SIRT3), a class III HDAC (39% SIRT3 inhibition at 200 μM). Upregulation of SIRT3 transcription is associated with oral squamous cell carcinoma (OSCC) and breast cancer with lymph node involvement, while SIRT3 down-regulation inhibits the growth of OSCC cells and sensitizes them to radiation and chemotherapy.

CAY10722 is an inhibitor of sirtuin 3 (SIRT3), a class III HDAC (71% inhibition at 200 μM). SIRT3 is involved in modulating metabolic homeostasis as a NAD+-dependent protein deacetylase in the mitochondria. SIRT3 functions as either an oncogene or tumor suppressor, depending on cancer cell type. High SIRT3 expression in patient-derived esophageal cancer tissues is associated with shorter survival and, in mice, downregulation leads to a lower tumor load. In contrast, low SIRT3 expression in patient-derived breast cancer cells is correlated with shorter survival.

Mn(III)TMPyP is a manganese-porphyrin which acts as a superoxide dismutase (SOD) mimetic and peroxynitrite decomposition catalyst. SOD mimetics described to date are unstable and are capable of catalyzing undesired side-reactions in addition to the dismutation of the superoxide radical (O2-). Mn(III)TMPyP is an SOD mimetic with increased stability to pH and hydrogen peroxide. The rate constant for superoxide dismutation and peroxynitrite decomposition are 3.9 x 107 M-1s-1 and ~2 x 106 M-1s-1, respectively. Mn(III)TMPyP protected and enhanced the growth of SOD E. coli with a doubling time of 60 minutes (as compared to 240 minutes of the control) at 25 µM.

Urocortin II is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin III , frog sauvagine, and piscine urotensin I.1 Mouse urocortin II shares 34 and 42% sequence homology with rat CRF and urocortin . It is expressed in mouse paraventricular, supraoptic, and arcuate nuclei of the hypothalamus, the locus coeruleus, and in motor nuclei of the brainstem and spinal ventral horn. Urocortin II selectively binds to CRF1 over CRF2 receptors (Kis = 0.66 and >100 nM, respectively) and induces cAMP production in CHO cells expressing CRF2 (EC50 = 0.14 nM). In vivo, urocortin II suppresses nighttime food intake by 35% in rats when administered intracerebroventricularly at a dose of 1 μg. Urocortin II (0.1 and 0.5 μg, i.c.v) stimulates fecal pellet output, increases distal colonic transit, and inhibits gastric emptying in mice.2References1. Reyes, T.M., Lewis, K., Perrin, M.H., et al. Urocortin II: A member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by type 2 CRF receptors. Proc. Natl. Acad. Sci. U.S.A. 98(5), 2843-2848 (2001).2. Martinez, V., Wang, L., Million, M., et al. Urocortins and the regulation of gastrointestinal motor function and visceral pain. Peptides 25(10), 1733-1744 (2004). Urocortin II is a neuropeptide hormone and member of the corticotropin-releasing factor (CRF) family which includes mammalian CRF , urocortin , urocortin III , frog sauvagine, and piscine urotensin I.1 Mouse urocortin II shares 34 and 42% sequence homology with rat CRF and urocortin . It is expressed in mouse paraventricular, supraoptic, and arcuate nuclei of the hypothalamus, the locus coeruleus, and in motor nuclei of the brainstem and spinal ventral horn. Urocortin II selectively binds to CRF1 over CRF2 receptors (Kis = 0.66 and >100 nM, respectively) and induces cAMP production in CHO cells expressing CRF2 (EC50 = 0.14 nM). In vivo, urocortin II suppresses nighttime food intake by 35% in rats when administered intracerebroventricularly at a dose of 1 μg. Urocortin II (0.1 and 0.5 μg, i.c.v) stimulates fecal pellet output, increases distal colonic transit, and inhibits gastric emptying in mice.2 References1. Reyes, T.M., Lewis, K., Perrin, M.H., et al. Urocortin II: A member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by type 2 CRF receptors. Proc. Natl. Acad. Sci. U.S.A. 98(5), 2843-2848 (2001).2. Martinez, V., Wang, L., Million, M., et al. Urocortins and the regulation of gastrointestinal motor function and visceral pain. Peptides 25(10), 1733-1744 (2004).

L-AP4 (L-APB) monohydrate is a potent and specific agonist for the group III mGluRs, with EC50s of 0.13, 0.29, 1.0, 249 μM for mGlu4, mGlu8, mGlu6 and mGlu7 receptors, respectively[1][2]. L-AP4 (5-30 μg, intrathecal inhection 4-5 days) significantly increases the paw withdrawal threshold in response to application of von Frey filaments in eight nerve-ligated rats in a dose-dependent manner. Intrathecal administration of different doses of L-AP4 is not associated with any evident motor dysfunction[2].Intrathecal injection of 30 μg of L-AP4 does not significantly alter the paw withdrawal latency in these normal rats[2].Topical application of 5 to 50 μM L-AP4 to the spinal cord significantly inhibited the evoked response of neurons to touch, pressure, pinch, and von Frey filaments in a concentration-dependent fashion[2]. Animal Model: Rats.[2] [1]. Selvam C, et al. Increased Potency and Selectivity for Group III Metabotropic Glutamate Receptor Agonists Binding at Dual sites. J Med Chem. 2018 Mar 8;61(5):1969-1989. [2]. Chen SR, et al. Distinct roles of group III metabotropic glutamate receptors in control of nociception and dorsal horn neurons in normal and nerve-injured Rats. J Pharmacol Exp Ther. 2005 Jan;312(1):120-6.

Antimycin A4 is an active component of the antimycin A antibiotic complex that is more polar than antimycin A1 , antimycin A2 , and antimycin A3 . Antimycin A4 inhibits ATP-citrate lyase with a Ki value of 64.8 μM. The antimycin A complex is a mixture of antimycins A1, A2, A3, and A4 that demonstrates antifungal, insecticidal, nematocidal, and piscicidal properties. It blocks mitochondrial respiration and can deplete cellular levels of ATP via inhibition of complex III of the mitochondrial electron transport chain (ETC). Antimycin A prevents the transfer of electrons between the b-cytochromes and ubiquinone at the Q(inner) site of complex III. This results in the stabilization of the ubisemiquinone radical at the Q(outer) site of complex III, leading to increased production of superoxide. Antimycin A is widely used in research to shunt electron flow through the ETC to study the chemical details of oxygen respiration. Additionally, antimycin A has been shown to inhibit Bcl-2 and Bcl-xL proteins, inducing apoptosis.

Chlorido[N,N'-disalicylidene-1,2-phenylenediamine]iron(III) 是一种具有潜在光敏活性的席夫碱-铁(III)络合物。它在特定波长的光照下能高效催化细胞内活性氧 (ROS) 的爆发，通过诱导严重的氧化损伤和线粒体功能障碍触发肿瘤细胞的凋亡。

H-D-Phe-Pip-Arg-pNA hydrochloride, a chromogenic substrate, mimics the N-terminal segment of the A alpha chain of fibrinogen, the native substrate of thrombin. It displays specificity towards thrombin and is employed for quantifying antithrombin-heparin cofactor (AT-III). The utilization of H-D-Phe-Pip-Arg-pNA hydrochloride in the AT-III assay enables a sensitive, accurate, and straightforward measurement process.

FNDR-20123 是一个安全的、有效的抗疟疾 HDAC 抑制剂，能够作用于疟原虫 HDAC (IC50: 31 nM) 和人类 HDAC (IC50: 3 nM)。FNDR-20123 对恶性疟原虫 (Plasmodium falciparum) 无性期和性血期 (雄性配子体) 都显示出抗疟疾效果，其 IC50 值分别为 41 nM 和 190 nM。FNDR-20123 能够抑制 HDAC1 (IC50: 25 nM)、HDAC2 (IC50: 29 nM)、HDAC3 (IC50: 2 nM)、HDAC6 (IC50: 11 nM)、HDAC8 (IC50: 282 nM)，而且在纳摩尔浓度下可以抑制 III 类 HDAC 亚型。

Dilmapimod tosylate is a potent p38 mitogen-activated protein kinase (MAPK) inhibitor. It was investigated for its anti-inflammatory effect in non-head injury trauma patients at risk for developing acute respiratory distress syndrome. IL-1β was identified as a gene regulated by dilmapimod that could influence c-reactive protein levels. Dilmapimod had been in phase III clinical trials by GlaxoSmithKline for the treatment of rheumatoid arthritis, neuropathic pain, coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD).