更新于：2024-05-01
SLC22A2
solute carrier family 22 member 2
更新于：2024-05-01
基本信息
别名 hOCT2、OCT2、Organic cation transporter 2 + [3] |
简介 Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics (PubMed:9260930, PubMed:9687576). Functions as a Na(+)-independent, bidirectional uniporter (PubMed:9687576, PubMed:21128598). Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient (PubMed:9260930, PubMed:9687576, PubMed:15212162). However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (PubMed:15783073). Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters (PubMed:9687576, PubMed:16581093, PubMed:17460754). Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system (PubMed:17460754). Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium (PubMed:15817714). Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) (PubMed:9260930, PubMed:12089365, PubMed:15212162, PubMed:17072098, PubMed:24961373). Mediates the uptake and efflux of quaternary ammonium compound choline (PubMed:9260930). Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine (PubMed:12538837, PubMed:21128598). Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) (PubMed:11907186). Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) (PubMed:12395288, PubMed:16394027). May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable).
In contrast with isoform 1, not able to transport guanidine, creatinine, cimetidine and metformin. |
关联
100 项与 SLC22A2 相关的临床结果
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100 项与 SLC22A2 相关的转化医学
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0 项与 SLC22A2 相关的专利（医药）
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621
项与 SLC22A2 相关的文献（医药）2024-02-16·Pharmaceutics
Dysregulation of the mRNA Expression of Human Renal Drug Transporters by Proinflammatory Cytokines in Primary Human Proximal Tubular Epithelial Cells.
Article
作者: Yik Pui Tsang ; Tianran Hao ; Qingcheng Mao ; Edward J Kelly ; Jashvant D Unadkat
Proinflammatory cytokines, which are elevated during inflammation or infections, can affect drug pharmacokinetics (PK) due to the altered expression or activity of drug transporters and/or metabolizing enzymes. To date, such studies have focused on the effect of cytokines on the activity and/or mRNA expression of hepatic transporters and drug-metabolizing enzymes. However, many antibiotics and antivirals used to treat infections are cleared by renal transporters, including the basal organic cation transporter 2 (OCT2), organic anion transporters 1 and 3 (OAT1 and 3), the apical multidrug and toxin extrusion proteins 1 and 2-K (MATE1/2-K), and multidrug resistance-associated protein 2 and 4 (MRP2/4). Here, we determined the concentration-dependent effect of interleukin-6 (IL-6), IL-1β, tumor necrosis factor (TNF)-α, and interferon-γ (IFN-γ) on the mRNA expression of human renal transporters in freshly isolated primary human renal proximal tubular epithelial cells (PTECs, n = 3-5). PTECs were exposed to either a cocktail of cytokines, each at 0.01, 0.1, 1, or 10 ng/mL or individually at the same concentrations. Exposure to the cytokine cocktail for 48 h was found to significantly downregulate the mRNA expression, in a concentration-dependent manner, of OCT2, the organic anion transporting polypeptides 4C1 (OATP4C1), OAT4, MATE2-K, P-glycoprotein (P-gp), and MRP2 and upregulate the mRNA expression of the organic cation/carnitine transporter 1 (OCTN1) and MRP3. OAT1 and OAT3 also appeared to be significantly downregulated but only at 0.1 and 10 ng/mL, respectively, without a clear concentration-dependent trend. Among the cytokines, IL-1β appeared to be the most potent at down- and upregulating the mRNA expression of the transporters. Taken together, our results demonstrate for the first time that proinflammatory cytokines transcriptionally dysregulate renal drug transporters in PTECs. Such dysregulation could potentially translate into changes in transporter protein abundance or activity and alter renal transporter-mediated drug PK during inflammation or infections.
2024-02-07·Drug metabolism and disposition: the biological fate of chemicals
Use of a Double-Transfected System to Predict hOCT2/hMATE1-mediated Renal Drug-drug Interactions.
Article
作者: Letícia S Vieira ; Joanne Wang
Accurate predictions of renal drug-drug interactions (DDIs) mediated by the human organic cation transporter 2 (hOCT2) and multidrug and toxin extrusion proteins (hMATEs) remain challenging. Current DDI evaluation using plasma maximal unbound inhibitor concentrations (Imax,u) and IC50 values determined in single transporter-transfected cells frequently leads to false or overprediction especially for hMATE1. Emerging evidence suggests intracellular unbound inhibitor concentration may be more relevant for hMATE1 inhibition in vivo. However, determination of intrarenal inhibitor concentrations is impractical. Here we explored the use of hOCT2/hMATE1 double-transfected MDCK cells as a new in vitro tool for DDI risk assessment. Our results showed that potent in vitro hMATE1 inhibitors (hydroxychloroquine, brigatinib and famotidine) failed to inhibit metformin B-to-A flux in the double-transfected system. On the other side, the classical hOCT2/hMATE1 inhibitors, pyrimethamine and cimetidine, dose-dependently inhibited metformin apparent B-to-A permeability (Papp). The different behaviors of these hMATE1 inhibitors in the double-transfected system can be explained by their different ability to gain intracellular access either via passive diffusion or transporter-mediated uptake. A new parameter (IC50,flux) was proposed reflecting the inhibitor's potency on overall hOCT2/hMATE1-mediated tubular secretion. The IC50,flux values significantly differ from the IC50 values determined in single transporter-transfected cells. Importantly, the IC50,flux accurately predicted in vivo DDIs (within 2-fold) when used in a static model. Our data demonstrated that the IC50,flux approach circumvents the need to measure intracellular inhibitor concentrations and more accurately predicted hOCT2/hMATE1-mediated renal DDIs. This system represents a new approach that could be used for improved DDI assessment during drug development. Significance Statement This study demonstrated that flux studies in double-transfected MDCK cells and the IC50,flux represents a better approach to assess in vivo DDI potential for the renal organic cation secretion system. Our study highlights the importance of inhibitor intracellular accessibility for accurate prediction of hMATE1-mediated renal DDIs. This approach has the potential to identify in vitro hMATE1 inhibitors that are unlikely to result in in vivo DDIs, thus reducing the burden of unnecessary and costly clinical DDI investigations.
2024-02-02·Drug metabolism and disposition: the biological fate of chemicals
Interaction and Transport of Benzalkonium Chlorides (BACs) by the Organic Cation and Multidrug and Toxin Extrusion Transporters.
Article
作者: Letícia S Vieira ; Ryan P Seguin ; Libin Xu ; Joanne Wang
Humans are chronically exposed to benzalkonium chlorides (BACs) from environmental sources. The FDA has recently called for additional BAC safety data, as these compounds are cytotoxic and with great potential for biochemical interactions. Biodistribution studies revealed that BACs extensively distribute to many tissues and accumulate at high levels, especially in the kidneys, but the underlying mechanisms are unclear. In this study, we characterized the interactions of BACs of varying alkyl chain length (C8 to C14) with the human organic cation transporters (hOCT1-3) and multidrug and toxin extrusion proteins (hMATE1/2K) with the goal to identify transporters that could be involved in BAC disposition. Using transporter-expressing cell lines, we showed that all BACs are inhibitors of hOCT1-3 and hMATE1/2K (IC50 ranging 0.83-25.8 µM). Further, the short-chain BACs (C8 and C10) were identified as substrates of these transporters. Interestingly, while BAC C8 displayed typical Michaelis-Menten kinetics, C10 demonstrated a more complex substrate-inhibition profile. Transwell studies with transfected Madin-Darby canine kidney cells revealed that intracellular accumulation of basally applied BAC C8 and C10 was substantially higher (8.2- and 3.7-fold, respectively) in hOCT2/hMATE1 double-transfected cells in comparison to vector-transfected cells, supporting a role of these transporters in mediating renal accumulation of these compounds in vivo. Together, our results suggest that BACs interact with hOCT1-3 and hMATE1/2K as both inhibitors and substrates, and that these transporters may play important roles in tissue-specific accumulation and potential toxicity of short-chain BACs. Our findings have important implications for understanding human exposure and susceptibility to BACs due to environmental exposure. Significance Statement Humans are systemically exposed to BACs. These compounds broadly distribute through tissues, and their safety has been questioned by the FDA. Our results demonstrate that hOCT2 and hMATE1 contribute to the renal accumulation of BAC C8 and C10, and that hOCT1 and hOCT3 may be involved in the tissue distribution of these compounds. These findings can improve our understanding of BAC disposition and toxicology in humans, as their accumulation could lead to biochemical interactions and deleterious effects.
15
项与 SLC22A2 相关的新闻（医药）2024-03-21
·今日头条
本文为转化医学网原创，转载请注明出处
作者：Jerry
导读：
多年来，二甲双胍作为治疗2型糖尿病的首选药物，为众多患者带来了健康的福音与生命的希望。除了在治疗糖尿病方面取得显著成效，二甲双胍还在抗肿瘤、抗焦虑、延缓衰老、保护心血管、提升认知功能以及改善牙周病等多个方面展现出令人瞩目的影响。
2024 年 3 月 15 日，清华大学刘翔宇研究员、陈立功研究员、闫创业研究员（曾经师从施一公）等多个团队联合在 《Cell Discovery 》杂志发表题为“ Structural insights into human organic cation transporter 1 transport and inhibition”的研究论文。该研究获得了分辨率高达 2.98 Å 至 4.14 Å， hOCT1 与二甲双胍复合物在不同构象状态下的三维结构，捕捉到 hOCT1 跨膜转运二甲双胍的全过程。
通过结构生物学和生物化学相结合的手段阐明 hOCT1 转运底物二甲双胍的机制，揭示了螺内酯及甾醇类小分子的抑制机理，为精准靶向二甲双胍转运蛋白 hOCT1 的药物设计提供了新的理论基础！
https://www.nature.com/articles/s41421-024-00664-1
研究背景
01
人有机阳离子转运体 1（hOCT1），也被称为 SLC22A1，是肝脏摄取内源性和外源性有机阳离子不可或缺的一部分，影响并参与代谢过程、药代动力学和药效动力学。二甲双胍是一种重要的 hOCT1 底物。在降糖机制方面，二甲双胍主要通过 hOCT1(SLC22A1) 进入肝脏细胞，激活 AMPK 信号通路，抑制肝糖原的输出。
研究结果
02
研究团队阐明了 hOCT1 与二甲双胍复合物的结构，其跨越三种构象：向外开放（hOCT1-M1）、向外封闭（hOCT1-M2）和向内封闭（hOCT1-M3），以及具有向内开放构象的未结合的 hOCT1。
在向外开放状态下，hOCT1二甲双胍结合位点暴露在细胞外。连接细胞外环境到结合位点的通道带负电荷，可能增强对带正电荷有机阳离子底物的选择性。二甲双胍位于中央腔内，与TM7上的Y361形成阳离子-π相互作用，Q362也可能有助于底物结合。从向外开放到闭合状态的转变以CTD螺旋的细胞外端的移动为特征，这些螺旋的细胞内部分表现出最小的位移。这导致通道变窄，螺旋TM9、TM10、TM11、TM12向腔内汇聚，然后TM7靠近中央腔移动约1.5 A。这些构象变化促进Y361的轻微内移，缩小了细胞外通道，并导致二甲双胍向NTD方向轻微移动。
在从向外封闭状态至向内封闭状态转变的过程中，CTD螺旋的胞外端和胞内端都发生了显著的重排。TM7经历了额外的向内运动，胞外端从环向螺旋结构过渡，并使二甲双胍更接近由NTD的F32、F244和W217组成的芳香残基束。突变这些芳香残基抑制了hOCT1对二甲双胍的转运，表明维持Y361和二甲双胍之间的阳离子-π相互作用的重要性。
从向内封闭状态到向内开放状态的最终转变标志着CTD螺旋的胞内端进一步运动，形成一个完全开放的通道，连接中央腔和细胞质。在这个过程中，这些螺旋的胞外端大部分保持静止。W354经历了侧链旋转，该位点的突变影响二甲双胍转运。
至此，研究团队总结出 hOCT1 底物转运过程中，由 YER 基序参与的构象变化机制，并解释了部分由 hOCT1 基因多态性所引起底物转运能力降低的可能机制。
另外，研究人员还进一步研究了螺内酯和相关类固醇激素对hOCT2和hOCT3的抑制作用，这些激素具有与hOCT1类似的结合口袋结构。
一致地，所有三种化合物(螺内酯、孕酮和雌二醇)都抑制了hOCT2和hOCT3底物转运。其中，孕酮是最强的hOCT2抑制剂。
螺内酯抑制hOCT1的分子机制
研究结论
03
本研究报道了hOCT1底物结合口袋在不同构象下的高分辨率结构，并详细阐述了hOCT1在底物转运过程中经历的多种构象变化，进一步确定了“YER”基序对hOCT1正常功能至关重要。
本研究结果为精准设计 hOCT1 相关药物提供了新的理论依据！
参考资料：
https://www.nature.com/articles/s41421-024-00664-1
注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。
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2024-03-18
·生物探索
引言人类有机阳离子转运蛋白1（hOCT1），也称为SLC22A1，是肝脏摄取结构多样的内源性和外源性有机阳离子的重要蛋白，影响着代谢和药物的药代动力学。hOCT1已被认为在许多药物的治疗动力学中起着关键作用，使与hOCT1的相互作用成为新药开发和药物相互作用的重要考虑因素。值得注意的是，二甲双胍，作为2型糖尿病的前线药物，是一种突出的hOCT1底物。相反，hOCT1可以被类似醛固酮受体的类固醇类拮抗剂阿利多醇等药物抑制，这需要深入了解hOCT1与药物的相互作用，在新药物治疗的开发中起到至关重要的作用。尽管进行了大量研究，但在分子水平上，hOCT1转运和抑制机制的具体细节仍然难以捉摸。2024年3月15日，清华大学刘翔宇、陈立功及闫创业共同通讯在Cell Discovery（IF 34）在线发表题为“Structural insights into human organic cation transporter 1 transport and inhibition”的研究论文，该研究提出了hOCT1-二甲双胍复合物的冷冻电子显微镜结构，显示了三种不同构象状态——向外开放、向外阻塞和向内阻塞，以及部分和完全开放状态下的无底物hOCT1。该研究还提出了hOCT1与阿利多醇在向外和向内构象状态下的复合物。这些结构提供了关于通过hOCT1进行二甲双胍转运的动态过程以及阿利多醇如何抑制它的机制的原子水平洞察力。此外，该研究确定了一个关键的“YER”基序，对hOCT1的构象灵活性以及可能对其他SLC22家族转运蛋白起作用。总之，该研究显著推进了对hOCT1分子功能的理解，并为设计针对该转运蛋白的新治疗药物奠定了基础框架。许多药物和内源性分子在细胞和细胞器膜之间的转运是由转运蛋白促进的。在这些转运蛋白中，有机阳离子转运蛋白OCT1（SLC22A1），作为SLC22家族的成员，在肝脏中表达较多，并于1994年首次被鉴定出来。OCT1已被确定为多种药理学上重要药物的关键肝脏转运蛋白，包括二甲双胍、抗癌药奥沙利铂和阿片类药物吗啡。OCT1还被认为高容量地转运硫胺素，通过调节细胞能量状态来调节肝脏脂肪变性，并作为一种神经递质转运蛋白，控制循环儿茶酚胺水平。hOCT1的功能影响着许多药物的药代动力学，药物基因组学研究表明，影响hOCT1活性的基因多态性可能改变药物的效果，有时会导致不良反应。尽管hOCT1是主要的肝脏转运蛋白，但hOCT家族成员hOCT2和hOCT3在肾脏和其他器官系统中也有作用。尽管其序列同源性较高，但OCT1、OCT2和OCT3在组织分布、底物特异性和药理学抑制方面存在明显差异，突显了它们独特的生理作用。对这些差异的清晰理解对于开发精准医学策略至关重要。参与hOCT1构象变化的3个关键残基（Credit: Cell Discovery）作为主要促进子超家族（MFS）的一部分，hOCT1通过交替进入机制运作，通过转运蛋白构象变化，将底物结合位点交替暴露于膜的两侧。每个hOCT1转运周期涉及从向外开放到向外阻塞，然后是向内阻塞，最后是向内开放状态的转变。尽管最近通过研究hOCT3的向外构象、OCT1cs和OCT2cs的一致突变来定义了转运机制的进展，但动态的底物转运过程仍然不明确。为了完全定义转运机制，需要详细的hOCT1转型状态的结构信息。该研究阐明了hOCT1与二甲双胍复合物的冷冻电子显微镜结构，捕捉了三种关键的构象状态，以及在向内开放状态下的无底物hOCT1。此外，该研究展示了hOCT1与抑制剂阿利多醇结合的结构，揭示了hOCT1的转运和抑制的分子机制。原文链接https://doi.org/10.1038/s41421-024-00664-1责编|探索君排版|探索君文章来源|“iNature”End往期精选围观一文读透细胞死亡(Cell Death) | 24年Cell重磅综述（长文收藏版）热文Nature | 破除传统：为何我们需要重新思考肿瘤的命名方式热文Nature | 2024年值得关注的七项技术热文Nature | 自身免疫性疾病能被治愈吗？科学家们终于看到了希望热文CRISPR技术进化史 | 24年Cell综述
2024-03-14
WASHINGTON, March 14, 2024 (GLOBE NEWSWIRE) -- 60 Degrees Pharmaceuticals, Inc., (NASDAQ: SXTP, SXTPW) (“60 Degrees Pharmaceuticals” or the “Company”), a pharmaceutical company focused on developing new medicines for infectious diseases, today announced that the U.S. Food and Drug Administration (FDA) has communicated its intention to send any comments regarding the Company’s babesiosis trial within the month of April, 2024, rather than March, 2024 as anticipated by the Company. The protocol submission mechanism as directed by the FDA, i.e., under the Company’s existing (rather than a new) Investigational New Drug application, technically does not require a response from the FDA within a specified time frame.
The Company is continuing preparations for a June 1, 2024 start date as previously communicated.
Tafenoquine is the active ingredient in an anti-malarial approved by the FDA in 2018 and is indicated for the prophylaxis of malaria in patients aged 18 years of age and older.
About ARAKODA® (tafenoquine)
Tafenoquine was discovered by Walter Reed Army Institute of Research. Tafenoquine was approved for malaria prophylaxis in 2018 in the United States as ARAKODA® and in Australia as KODATEF®. Both were commercially launched in 2019 and are currently distributed through pharmaceutical wholesaler networks in each respective country. They are available at retail pharmacies as a prescription-only malaria prevention drug.
According to the Centers for Disease Control and Prevention, the long terminal half-life of tafenoquine, which is approximately 16 days, may offer potential advantages in less frequent dosing for prophylaxis for malaria. ARAKODA® is not suitable for everyone, and patients and prescribers should review the Important Safety Information below.
ARAKODA® (tafenoquine) Important Safety Information
ARAKODA® is an antimalarial indicated for the prophylaxis of malaria in patients aged 18 years of age and older.
Contraindications
ARAKODA® should not be administered to:
Patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency or unknown G6PD status.
Lactating women who are breastfeeding when the infant is found to be G6PD deficient or if G6PD status is unknown.
Patients with a history of psychotic disorders or current psychotic symptoms.
Patients with known hypersensitivity reactions to tafenoquine, other 8-aminoquinolines or any component of ARAKODA®.
Warnings and Precautions
Hemolytic Anemia: G6PD testing must be performed before prescribing ARAKODA® due to the risk of hemolytic anemia. Monitor patients for signs or symptoms of hemolysis.
G6PD Deficiency in Pregnancy or Lactation: ARAKODA® may cause fetal harm when administered to a pregnant woman with a G6PD-deficient fetus. ARAKODA® is not recommended during pregnancy. A G6PD-deficient infant may be at risk for hemolytic anemia from exposure to ARAKODA® through breast milk. Check infant’s G6PD status before breastfeeding begins.
Methemoglobinemia: Asymptomatic elevations in blood methemoglobin have been observed. Initiate appropriate therapy if signs or symptoms of methemoglobinemia occur.
Psychiatric Effects: Serious psychotic adverse reactions have been observed in patients with a history of psychosis or schizophrenia, at doses different from the approved dose. If psychotic symptoms (hallucinations, delusions or grossly disorganized thinking or behavior) occur, consider discontinuation of ARAKODA® therapy and evaluation by a mental health professional as soon as possible.
Hypersensitivity Reactions: Serious hypersensitivity reactions have been observed with administration of ARAKODA®. If hypersensitivity reactions occur, institute appropriate therapy.
Delayed Adverse Reactions: Due to the long half-life of ARAKODA® (approximately 16 days), psychiatric effects, hemolytic anemia, methemoglobinemia and hypersensitivity reactions may be delayed in onset and/or duration.
Adverse Reactions: The most common adverse reactions (incidence greater than or equal to 1%) were: headache, dizziness, back pain, diarrhea, nausea, vomiting, increased alanine aminotransferase, motion sickness, insomnia, depression, abnormal dreams and anxiety.
Drug Interactions
Avoid co-administration with drugs that are substrates of organic cation transporter-2 or multidrug and toxin extrusion transporters.
Use in Specific Populations
Lactation: Advise women not to breastfeed a G6PD-deficient infant or infant with unknown G6PD status during treatment and for 3 months after the last dose of ARAKODA®.
To report SUSPECTED ADVERSE REACTIONS, contact 60 Degrees Pharmaceuticals at 1- 888-834-0225 or FDA at 1-800-FDA-1088 or . ARAKODA® full prescribing information is here.
About 60 Degrees Pharmaceuticals, Inc.
60 Degrees Pharmaceuticals, Inc., founded in 2010, specializes in developing and marketing new medicines for the treatment and prevention of infectious diseases that affect the lives of millions of people. 60 Degrees Pharmaceuticals achieved FDA approval of its lead product, ARAKODA® (tafenoquine) for malaria prevention, in 2018. 60 Degrees Pharmaceuticals also collaborates with prominent research organizations in the U.S., Australia and Singapore. The 60 Degrees Pharmaceuticals mission has been supported through in-kind funding from the United States Department of Defense and private institutional investors including Knight Therapeutics Inc., a Canadian-based pan-American specialty pharmaceutical company. 60 Degrees Pharmaceuticals is headquartered in Washington D.C., with a majority-owned subsidiary in Australia. Learn more at .
Cautionary Note Regarding Forward-Looking Statements
This press release may contain “forward-looking statements” within the meaning of the safe harbor provisions of the U.S. Private Securities Litigation Reform Act of 1995. Forward‐looking statements reflect the current view about future events. When used in this press release, the words “anticipate,” “believe,” “estimate,” “expect,” “future,” “intend,” “plan” or the negative of these terms and similar expressions, as they relate to us or our management, identify forward‐looking statements. Forward-looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, projections, anticipated events and trends, the economy and other future conditions. Because forward-looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. Our actual results and financial condition may differ materially from those indicated in the forward-looking statements. Therefore, you should not rely on any of these forward-looking statements. Important factors that could cause our actual results and financial condition to differ materially from those indicated in the forward-looking statements include, among others, the following: there is substantial doubt as to our ability to continue on a going-concern basis; we might not be eligible for Australian government research and development tax rebates; if we are not able to successfully develop, obtain FDA approval for, and provide for the commercialization of non-malaria prevention indications for tafenoquine (ARAKODA® or other regimen) or Celgosivir in a timely manner, we may not be able to expand our business operations; we may not be able to successfully conduct planned clinical trials; and we have no manufacturing capacity which puts us at risk of lengthy and costly delays of bringing our products to market. More detailed information about the Company and the risk factors that may affect the realization of forward-looking statements is set forth in the Company’s filings with the Securities and Exchange Commission (SEC), including our Annual Report on Form 10-K and our subsequent Quarterly Reports on Form 10-Q. Investors and security holders are urged to read these documents free of charge on the SEC’s web site at As a result of these matters, changes in facts, assumptions not being realized or other circumstances, the Company’s actual results may differ materially from the expected results discussed in the forward-looking statements contained in this press release. Any forward-looking statement made by us in this press release is based only on information currently available to us and speaks only as of the date on which it is made. We undertake no obligation to publicly update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.
Media Contacts:
Sheila A. Burke
SheilaBurke-consultant@60degreespharma.com
(484) 667-6330
Investor Contact:
Patrick Gaynes
patrickgaynes@60degreespharma.com
(310) 989-5666
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