balb/c

TAK-041 (NBI-1065846) 是一种选择性 GPR139激动剂，EC50为 22 nM，有用于精神分裂症阴性症状的研究潜力。

Capmatinib 2HCl (INC-280 2HCl) 是一种新型的 ATP 竞争性 c-MET 激酶抑制剂，IC50 为 0.13 nM。它具有皮摩尔酶效，对 c-MET 具有高度特异性，选择性超过 10, 000 倍一大组人类激酶。该抑制剂在 c-MET 依赖性肿瘤细胞系中有效阻断 c-MET 磷酸化和其关键下游效应子的激活。因此，它在体外有效抑制 c-MET 依赖性肿瘤细胞增殖和迁移，并有效诱导细胞凋亡。

Capmatinib xHCl (INCB28060) 是一种有效的、口服活性的、选择性的和 ATP 竞争性 c-Met 激酶抑制剂，有效地阻断体外激酶活性 (IC50 = 0.13 nM) 以及在细胞中的组成型或 HGF 刺激活性(IC50 值范围从 0.3 到1.1纳米)。

Capmatinib 2HCl.H2O (NVP-INC280 2HCl.H2O) 是一种具有潜在抗肿瘤活性的原癌基因 c-Met (HGFR) 的口服生物可利用抑制剂。

Oxiconazole nitrate (Ro 13-8996) 是广谱抗真菌药物，抑制T. tonsurans 和T.rubrum 的生长，MIC90值分别为 0.25 和 0.5 μg/mL。

Capmatinib (INCB28060) 是一种具有口服活性的，选择性的，ATP 竞争性的c-Met 激酶抑制剂，IC50值为0.13 nM。它有效抑制 c-Met 依赖性肿瘤细胞的增殖和迁移，可诱导细胞凋亡，有抗肿瘤活性。

Redaporfin, also known as F-2BMet or LUZ-11, is a photosensitizer for Photodynamic Therapy (PDT) of cancer. Redaporfin showed a high efficacy in the treatment of male BALB/c mice with subcutaneously implanted colon (CT26) tumours. Vascular-PDT with 1.5 mg

Traxanox 是一种可口服的利尿剂。Traxanox 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox 对抑制BALB/c小鼠抗体产生的恢复作用。

Traxanox TFA 是一种可口服的利尿剂。Traxanox TFA 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox TFA 对抑制BALB/c小鼠抗体产生的恢复作用。

FKB04，作为一种端粒重复结合因子2（TRF2）抑制剂，在肝癌研究领域显示出潜力。通过破坏肝癌细胞的端粒维持机制，FKB04 诱导端粒缩短和细胞衰老，因而引发 T 环缺陷，发挥抗肿瘤活性。此外，该化合物还能抑制人肝癌异种移植小鼠模型（Huh-7 细胞植入 BALB/c 小鼠）中的肿瘤生长。

WRN inhibitor 14 (compound S35) 是一种口服WRN抑制剂，具有抗癌活性，可抑制 BALB/c 裸鼠 SW48 异种移植模型中的肿瘤生长。

Mtb-IN-9 (Compound M1) 是一种特异性的Mtb抑制剂，能够抑制MtbFadD32和MtbFadD28的活性。在BALB/c鼠慢性感染模型中，此化合物降低了受感染巨噬细胞中Mtb的存活率，并减少了Mtb负担和结核肉芽肿，对结核病的研究具有潜在的应用前景。

SGK1-IN-6 (compound 12f) 是一种具有 IC50 值为 0.39 μM 的 SGK1 抑制剂。在 BALB/c 裸鼠的 PC3 异种移植模型中，SGK1-IN-6 有效抑制肿瘤生长，并且未产生任何可观察的毒性。

PROTACGPX4 degrader-4 是一种 GPX4 PROTAC 降解剂 (DC50: 5.32 nM)，能够抑制 RT4、T24 和 J82 癌细胞的活性，其 IC50 分别为 0.09、2.97 和 7.58 μM。该化合物可在 T24 和 RT4 细胞中增加脂质 ROS 水平并诱导铁死亡 (ferroptosis)。此外，PROTACGPX4 degrader-4 在 T24 荷瘤 BALB/c 裸鼠模型中展现抗肿瘤活性，可用于膀胱癌研究。

Reveromycin C是一种聚酮化合物，最初从链霉菌中提取，具有抗白色念珠菌的抗真菌活性，在pH 3和pH 7.4时的MIC分别为2.0和>500 μg/mL。Reveromycin C可抑制Balb/MK小鼠表皮细胞系中EGF诱导的有丝分裂原活性。它还能逆转肉瘤病毒转化的NRK大鼠肾细胞的形态（EC50=1.58 μg/mL），并抑制KB细胞和K562人慢性粒细胞白血病细胞的增殖，两者的IC50均为2.0 μg/mL。

Traxanox sodium 是一种可口服的利尿剂。Traxanox sodium 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox sodium 对抑制BALB/c小鼠抗体产生的恢复作用。

PtdIns-(3,4,5)-P3 (PIP3) serves as an anchor for the binding of signal transduction proteins bearing pleckstrin homology (PH) domains such as phosphatidylinositol 3-kinase (PI3K) or PTEN. Protein binding to PIP3 is important for cytoskeletal rearrangement and membrane trafficking and initiates an intricate signaling cascade that has been implicated in cancer. 3,5-dimethyl PIT-1 is a dimethyl analog of PIT-1, the selective inhibitor of PIP3/Akt PH domain binding, that is designed for more favorable solubility in vivo. 3,5-dimethyl PIT-1 inhibits PI3K/Akt signaling (IC50 = 27 μM), suppressing PI3K-PDK1-Akt-dependent phosphorylation, which has been shown to reduce cell viability and induce apoptosis in PTEN-deficient U87MG glioblastoma cells (IC50 = 36 μM). 4T1 breast cancer growth is significantly attenuated in BALB/c mice with a dose of 1 mg/kg of 3,5-dimethyl PIT-1 per day.

Benpyrine is a highly specific and orally active TNF-α inhibitor with a KD value of 82.1 μM. Benpyrine tightly binds to TNF-α and blocks its interaction with TNFR1, with an IC50 value of 0.109 μM. Benpyrine has the potential for TNF-α mediated inflammatory and autoimmune disease research[1]. Benpyrine (5-20 μM; 14 hours; RAW264.7 cells) pretreatment results in a dose-dependent decrease in the phosphorylation of IκBα in RAW264.7 cells (stimulated with 10 ng/mL TNF-α or 1 μg/mL LPS). Benpyrine abolishes the TNF-α-induced nuclear translocation of NF-κB/p65 in RAW264.7 cells[1].Benpyrine only blocks cell death induced by TNF-αWT and Y119A, and increases the cell survival rate up to 80%. Benpyrine does not obviously affect L57A- and Y59L-induced cytotoxicity in L929 cells[1]. Benpyrine (25-50 mg/kg; oral gavage; daily; for 2 weeks; Balb/c mice) treatment significantly relieves the symptoms of collagen-induced arthritis. Benpyrine dose-dependently decreases the levels of proinflammatory cytokines, such as IFN-γ, IL-1β and IL-6, and increases the concentration of the anti-inflammatory cytokine IL-10[1].Endotoxemia murine model shows that Benpyrine (25 mg/kg) could attenuate TNF-α-induced inflammation, thereby reducing liver and lung injury[1]. [1]. Weiguang Sun, et al. Discovery of an Orally Active Small Molecule TNF-α Inhibitor. J Med Chem. 2020 Jul 15.

Reveromycin A is the major component of a complex of spiroketal antibiotics isolated from Streptomyces sp. It inhibits the mitogenic activity of epidermal growth factor in Balb/MK cells (IC50 = 0.7 μg/ml), displays antiproliferative activity against human KB and K562 tumor cell lines (IC50s = 1.9 and 1.6 μg/ml, respectively), and demonstrates antifungal activity against C. albicans (MIC = 2 μg/ml at pH 3). Reveromycin A also has been shown to inhibit bone resorption by inducing apoptosis in osteoclasts with an IC50 value of 0.7 μM.

Reveromycin D is a bacterial metabolite originally isolated from Streptomyces. It inhibits EGF-induced mitogenic activity in Balb/MK cells and has pH-dependent antifungal activity against C. albicans (MICs = 2 and >500 μg/ml at pH 3 and 7.4, respectively). Reveromycin D also inhibits proliferation of KB and K562 cells (IC50s = 1.6 and 1.3 μg/ml, respectively).

Reveromycin B is a spiroketal bacterial metabolite originally isolated from Streptomyces. It inhibits EGF-induced mitogenic activity in Balb/MK cells (IC50 = 6 μg/ml) and exhibits pH-dependent antifungal activity against C. albicans (MICs = 15.6 and >500 μg/ml at pH 3.0 and 7.4, respectively). Unlike reveromycin A and reveromycin C , reveromycin B does not inhibit proliferation of KB and K562 cells.

Purfalcamine is an orally active, selective Plasmodium falciparum calcium-dependent protein kinase 1 (PfCDPK1) inhibitor with an IC50 of 17 nM and an EC50 of 230 nM. Purfalcamine has antimalarial activity and causes malaria parasites developmental arrest at the schizont stage[1][2]. Purfalcamine has low activity against Toxoplasma gondii calcium-dependent protein kinase 3 (TgCDPK3)[1]. Purfalcamine (225, 450 nM) has no effect on the parasitemia in the first 32 hours. After about 40 hours, parasite level remains stable and then begins dropping[1]. Purfalcamine inhibits proliferation with EC50s of 171-259 nM for P. falciparum strains (3D7, Dd2, FCB, HB3 and W2), which indicates effectiveness against drug-resistant parasites[1]. Given that the EC50 value for P. falciparum (3D7) is 230 nM, Purfalcamine shows a therapeutic window ranging from 23-fold to 36-fold (EC50s for CHO=12.33 μM, HEp2=7.235 μM, HeLa=7.029 μM and Huh7=5.476 μM)[1]. Purfalcamine (10 mg/kg; oral gavage; BID; for 6 days) demonstrates a delay in the onset of parasitemia in treated mice[1]. Purfalcamine (20 mg/kg; orally gavage) exhibits a Cmax of 2.6 μM with a half-life of 3.1 hours[1]. Animal Model: Male BALB/c mice, 7 weeks of age with the malaria parasite[1] [1]. Nobutaka Kato, et al. Gene expression signatures and small-molecule compounds link a protein kinase to Plasmodium falciparum motility. Nat Chem Biol. 2008 Jun;4(6):347-56. [2]. Rajshekhar Y Gaji, et al. Expression of the essential Kinase PfCDPK1 from Plasmodium falciparum in Toxoplasma gondii facilitates the discovery of novel antimalarial drugs. Antimicrob Agents Chemother. 2014 May;58(5):2598-607.

Tubulin polymerization-IN-6 (compound 5f) is a potent inhibitor of tubulin polymerization, with an IC50 of 1.09 μM. It not only inhibits cell migration and tube formation but also has anti-angiogenic properties. Additionally, Tubulin polymerization-IN-6 has been found to effectively hinder tumor growth in HT29 xenograft Balb/c nude mice [1].

Antitubercular agent-19 是一种抗结核剂。Antitubercular agent-19 对 MTB H37Rv 和 MDR-MTB 表现出良好的抗结核效果 (MIC＜0.016 μg/ml)。Antitubercular agent-19 在 BALB/c 小鼠中表现出较低的细胞毒性和相对较高的急性致死毒性。