由于齐考诺肽仅部分降低分化的人神经母细胞瘤 IMR32 细胞、大鼠颈上神经节神经元和大鼠海马神经元的高电压激活，这是因为大多数天然细胞携带许多不同的钙通道。钙流。此外，齐康米特还可减少 HEK 细胞、tsa-201 细胞和非洲爪蟾卵母细胞表达 α1B 亚基时产生的钙电流 [1]。通过降低脊髓背角中促伤害性神经递质的释放，齐考诺肽可阻断疼痛信号并具有抗伤害作用 [1]。

在脑脊髓炎 (EAE) 实验性自身免疫小鼠模型中，MOG35-55 触发 EAE 25 天后，脾脏中产生 IL-17 [2]。齐考诺肽（it；25-100 pmol/位点；5 μL；第 4、10、15、20 和 24 天）同样会降低 CNS 中的 IL-1β 和 IL-23 水平。

Animal/Disease Models: Female C57BL/6 mice (18-22 g, 6-8 weeks old) injected with myelin oligodendrocyte glycoprotein [2]
Doses: 25 pmol/site, 50 pmol/site, 100 pmol /site
Route of Administration: intrathecal injection; results on days 4, 10, 15, 20 and 24: Dramatically diminished mechanical hypersensitivity in EAE animals.

Absorption, Distribution and Excretion
Intrathecal ziconovide administered 1 hour later at doses of 1 to 10 mcg yielded calculated AUC values of 83.6–608 ngh/mL and Cmax values of 16.4–132 ng/mL; these values are approximately dose-proportional. Due to intrathecal administration and the small molecular size resulting in low membrane permeability, ziconovide is expected to be primarily found in cerebrospinal fluid; plasma concentrations (if detected) remain stable for up to nine months post-administration. A small amount of intravenously administered ziconovide (<1%) is excreted in the urine. In patients receiving 1–10 mcg of ziconovide intrathecally within 1 hour, the calculated apparent volume of distribution was 155 ± 263 mL; this is approximately equivalent to the expected cerebrospinal fluid volume. Although intravenous administration is not recommended, the apparent volume of distribution after intravenous administration of 0.3–10 mcg/kg/day of ziconovide is 30,460 ± 6366 mL.
The cerebrospinal fluid clearance rate of ziconovide was 0.38 ± 0.56 mL/min, and the plasma clearance rate was 270 ± 44 mL/min.
The concentration of ziconovide in brain tissue reached its peak at 0.003% to 0.006% per gram of tissue injection 3–20 minutes after intravenous injection, decreasing to below 0.001%/g after 2 hours. ...The peptide was perfused via an in vivo dialysis probe implanted in the hippocampus. Image analysis and serial sections showed minimal diffusion of ziconovide in the extracellular fluid surrounding the dialysis probe; the peptide remained within 1 mm of the probe after 2 hours. ...In situ perfusion via the carotid artery also confirmed the drug's entry into the brain from the bloodstream. Compared to 14C inulin, the amount of radioactive material crossing the blood-brain barrier after perfusion of radioiodine-labeled ziconovide was statistically significantly higher.
The pharmacokinetics and pharmacodynamics of ziconotide were evaluated within 48 hours following intrathecal injection (1, 5, 7.5, or 10 μg) in 22 patients with chronic non-malignant pain. Plasma and cerebrospinal fluid (CSF) samples were collected within 24 hours. Analgesic effect was monitored using the Visual Analogue Scale for Pain Intensity (VASPI) and the Classification of Pain Relief Scale (CPRS). Pharmacokinetic (PK) parameters were calculated using a non-compartmental model. Plasma ziconotide data were insufficient for pharmacokinetic calculations. In CSF, the median half-life of ziconotide was 4.5 hours. The median CSF clearance and volume of distribution were 0.26 mL/min and 99 mL, respectively. CSF pharmacokinetics of ziconotide showed a linear relationship based on cumulative exposure and peak CSF concentration. Dose-related analgesia was observed. …
Intrathecal injection of ziconotide causes almost no systemic exposure. After entering systemic circulation from cerebrospinal fluid (CSF), ziconopeptide is expected to be degraded into peptide fragments and their constituent amino acids by endopeptidases and exopeptidases present in most organs. Ziconopeptide binds to human plasma proteins at a rate of approximately 50%. Following intrathecal injection of ziconopeptide, its mean volume of distribution (Vd) in CSF is close to the estimated total CSF volume (140 mL). For more complete data on the absorption, distribution, and excretion of ziconopeptide (6 items), please visit the HSDB record page. Metabolism/Metabolites Ziconopeptide is expected to be metabolized by various peptidases after entering systemic circulation; detailed information on ziconopeptide metabolism is not currently available. Following intrathecal injection, ziconopeptide is rapidly distributed and/or metabolized in the spinal CSF, followed by relatively rapid transport of metabolites from CSF to plasma. The relative contributions of intraspinal and extraspinal transport and intraspinal metabolism are unclear. However, there is evidence that ziconopeptide can be rapidly transported into the bloodstream, and its metabolism within the spinal cord may play an important role. Once in the bloodstream, the compound is rapidly metabolized through normal proteolytic mechanisms, ultimately breaking down into its constituent amino acids; it can be inferred that these amino acids will be further metabolized or integrated into proteins through normal physiological processes. Ziconopeptide is cleaved at multiple sites on its peptide chain by endopeptidases and exopeptidases. During continuous intrathecal administration, after ziconopeptide enters the systemic circulation from the cerebrospinal fluid, it is expected to be rapidly degraded into peptide fragments and its constituent free amino acids by proteolytic cleavage by various peptidases/proteases commonly found in most organs (e.g., kidneys, liver, lungs, muscles, etc.). In vitro studies have shown that the hydrolytic activity of ziconopeptide in human and animal cerebrospinal fluid and blood is extremely low. The bioactivity of the various expected proteolytic degradation products of ziconopeptide has not been evaluated.

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Biological Half-Life
In patients who received intrathecal injections of 1–10 mcg of ziconopeptide within 1 hour, the calculated elimination half-life was 4.6 ± 0.9 hours. Although intravenous administration is not recommended, intravenous administration of ziconopeptide at doses of 0.3–10 mcg/kg/day results in an elimination half-life of 1.3 ± 0.3 hours. Following intrathecal administration, the terminal half-life of ziconopeptide in cerebrospinal fluid is approximately 4.6 hours (range 2.9–6.5 hours).

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
Currently, there is no information on the clinical use of ziconopeptide during lactation. After intrathecal injection, ziconopeptide is usually undetectable or only detectable in very small amounts in plasma, and due to its molecular weight of 2639 Daltons, the concentration in breast milk may be very low. Furthermore, ziconopeptide is likely to be partially destroyed in the infant's gastrointestinal tract, and the amount absorbed by the infant may be minimal. If the mother needs to use ziconopeptide, breastfeeding should not be discontinued. Sedation of breastfed infants should be monitored, as sedation may lead to respiratory depression or feeding difficulties.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
As of the revision date, no relevant published information was found.

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Protein Binding
Zicoconopeptide binds to human plasma proteins at a rate of approximately 50%.

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Interaction
Ziconovitide is a selective, potent, and reversible blocker of neuronal N-type voltage-sensitive calcium channels (VSCCs). Morphine is a μ-opioid receptor agonist that inhibits N-type VSCC channels via a G protein-coupled mechanism. Both drugs have analgesic effects when administered intrathecally (spinal cord). This study investigated the acute and chronic (7-day) interactions of intrathecal ziconovitide and morphine on nociceptive sensation in various animal models of pain. In the acute study, intrathecal administration of either morphine or ziconovitide alone dose-dependently inhibited formalin-induced tonic withdrawal and plantar pressure withdrawal responses. Combination administration of ziconovitide and morphine additively inhibited formalin-induced tonic withdrawal and significantly shifted the dose-response curve of morphine in the plantar pressure test to the left. Following chronic (7-day) intrathecal infusion, ziconovitide enhanced the analgesic effect of morphine in the formalin test. Conversely, chronic intrathecal morphine infusion can induce analgesia tolerance but does not affect the nociceptive effect of ziconovide. The analgesic effect of ziconovide alone is the same as that observed when ziconovide is co-administered with morphine in morphine-tolerant rats. In hot plate and tail dip tests, chronic intrathecal morphine infusion led to rapid tolerance, while ziconovide produced sustained analgesia without diminishing efficacy throughout the infusion. Although the co-administration of ziconovide and morphine produced significant synergistic analgesia in the initial phase of sustained infusion, it did not prevent the development of morphine analgesia tolerance. These results suggest that: (1) acute intrathecal ziconovide and morphine can produce additive or synergistic analgesia; (2) chronic intrathecal morphine infusion leads to analgesia tolerance but does not produce cross-tolerance to ziconovide; (3) long-term intrathecal ziconovide infusion does not produce tolerance or cross-tolerance to morphine analgesia; and (4) intrathecal ziconovide infusion does not prevent or reverse morphine tolerance. In clinical studies, ziconopeptide can be used in combination with anticonvulsants, antidepressants, antipsychotics, anxiolytics, and sedatives. It may interact with central nervous system depressants (increasing the incidence of adverse central nervous system reactions, such as dizziness, confusion, and decreased level of consciousness). Dosage adjustment or discontinuation of ziconopeptide or any concomitant central nervous system depressants may be necessary. It may also interact with antidepressants or anticonvulsants (increasing serum creatine kinase [CK, creatine phosphokinase, CPK]).

[1]. Ziconotide: a review of its pharmacology and use in the treatment of pain. Neuropsychiatr Dis Treat. 2007 Feb;3(1):69-85.

[2]. Beneficial Effects of the Calcium Channel Blocker CTK 01512-2 in a Mouse Model of Multiple Sclerosis. Mol Neurobiol. 2018 Dec;55(12):9307-9327.

Ziconotide (also known as SNX-111) is a neurotoxic peptide derived from the cone snail (Conus magus), composed of 25 amino acids and containing three disulfide bonds. Other similar peptides, collectively known as conotoxins, also exist, some of which have been shown to effectively bind to specific calcium channel subsets; ziconotide is used in part because its synthesis does not result in the loss of correct bonds or structural elements. Ziconotide is used to treat severe chronic pain unresponsive to other methods by inhibiting N-type calcium channels involved in nociceptive signaling. On December 28, 2004, ziconotide was approved by the U.S. Food and Drug Administration (FDA) and marketed by TerSera Therapeutics LLC. under the brand name Prialt. To date, ziconotide is the only calcium channel blocking peptide approved by the FDA. Ziconotide is a synthetic non-opioid multibasic peptide composed of 25 amino acids, an analogue of ω-conotoxin derived from the marine snail Conus magus, and possesses analgesic activity. Ziconovide appears to block neuronal N-type voltage-sensitive calcium channels (NCCBs), thereby inhibiting transmission from primary nociceptors in pain receptors. This drug may have significant analgesic effects on treatment-resistant pain.
See also: Ziconovide acetate (salt form).
Indications
Ziconovide is indicated for the treatment of patients with severe chronic pain unresponsive to other treatments and requiring intrathecal analgesia.
Ziconovide is indicated for the treatment of patients with severe chronic pain requiring intrathecal (IT) analgesia.
Mechanism of Action
Nociceptive pain signaling is a complex processing pathway involving peripheral nociceptors, primary afferent nerve fibers, and downstream central nervous system neurons in the spinal cord. Voltage-gated calcium channels (VGCCs) are important regulatory components of neural signaling, including N-type (Cav2.2) heteropolymer high-voltage calcium channels. Chronic pain, including inflammatory and neuropathic pain, typically involves the aberrant upregulation of voltage-gated calcium channel (VGCC) activity. This upregulation can be achieved through multiple cellular mechanisms and can lead to hyperalgesia and hyperalgesia. Specifically, activation of N-type channels is known to mediate the release of neurotransmitters substance P (SP), calcitonin gene-related peptide (CGRP), and glutamate in less myelinated Aδ and C fibers. These neurotransmitters affect downstream neural activation and pain perception. Furthermore, SP and CGRP can induce inflammation, potentially exacerbating pre-existing inflammatory chronic pain. Ziconotoxin, a neurotoxic peptide belonging to the ω-conotoxin class derived from the cone snail (Conus magus), inhibits N-type VGCCs. Although its exact mechanism is not fully elucidated, it is generally believed that ω-conotoxins act by directly blocking ion pores, preventing transmembrane transport of calcium ions. Further studies involving chimeric subunit expression and molecular modeling have shown that inserting the Met12 residue of ziconopeptide into the hydrophobic pocket formed by the Ile300, Phe302, and Leu305 residues of Cav2.2 enhances its binding affinity and may be associated with adverse toxicity. Ziconopeptide is an N-type calcium channel blocker (NCCB). Voltage-gated calcium channel (VSCC) transmission plays a crucial role in pain transmission. N-type VSCCs are present in high concentrations in dorsal root ganglion cells responsible for spinal cord pain processing. Ziconopeptide selectively and reversibly binds to and blocks these channels without interacting with other ion channels or cholinergic, monoaminergic, or μ and δ opioid receptors. Therefore, ziconopeptide inhibits spinal cord pain signal transduction.

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Therapeutic Use
Ziconotide intrathecal injection is used to treat severe chronic pain in patients who cannot tolerate or cannot obtain adequate analgesia from other therapies (e.g., systemic analgesics, adjunctive therapy, intrathecal morphine therapy), especially in cases requiring intrathecal treatment.

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Drug Warnings
/Black Box Warning/ Warning: Neuropsychiatric adverse reactions. Ziconotide is contraindicated in patients with a history of psychosis. Serious psychiatric symptoms and neurological dysfunction may occur during ziconotide treatment. All patients should be closely monitored for signs of cognitive impairment, hallucinations, or altered mood or consciousness. If severe neurological or psychiatric symptoms occur, ziconotide treatment should be discontinued. Meningitis has occurred in patients receiving ziconotide, primarily in patients treated via extracorporeal microinfusion devices and catheters. Meningitis may be due to accidental contamination of the microinfusion device or due to hematogenous or direct transmission of cerebrospinal fluid (e.g., from an infected pump or catheter access). Patients should be monitored for signs and symptoms of meningitis (e.g., fever, headache, neck stiffness, altered mental status, nausea or vomiting, seizures). Preparation of ziconopeptide solution and infusion of the drug reservoir should be performed by trained and qualified personnel under aseptic conditions. If meningitis is suspected (especially in immunocompromised patients) or confirmed, appropriate measures should be taken immediately (cerebrospinal fluid culture, anti-infective therapy, removal of the microinfusion device and catheter).
The use of Prialt has been associated with central nervous system-related adverse events, including psychiatric symptoms, cognitive impairment, and decreased alertness/slowed reaction time. In 1254 patients treated in clinical trials, the reported incidence of cognitive adverse events was as follows: confusion (33%), memory impairment (22%), speech impairment (14%), aphasia (12%), thought disorders (8%), and amnesia (1%). Cognitive impairment may gradually develop over several weeks of treatment. If signs or symptoms of cognitive impairment occur, the dose of Prialt should be reduced or the drug discontinued, but other possible causes should also be considered. The various cognitive effects of ziconovide are usually reversible within 2 weeks after discontinuation. The median recovery time for various cognitive effects is 3 to 15 days. Older adults (≥65 years) are at higher risk of confusion. Cognitive impairment (e.g., confusion, memory impairment, speech impairment, aphasia, thought disorders, amnesia) has been reported in patients treated with ziconovide. Cognitive impairment may develop gradually over several weeks and is usually reversible upon discontinuation. If cognitive impairment occurs, the dose of ziconovide should be reduced or discontinued; other possible causes of cognitive impairment should be considered. For more complete data on ziconovide (17 in total), please visit the HSDB record page.

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Pharmacodynamics
Ziconovide inhibits N-type calcium channels involved in nociceptive signaling, primarily acting on the dorsal horn of the spinal cord. Although binding is reversible, caution should be exercised to ensure efficacy and minimize adverse reactions, and ziconovide has a narrow therapeutic window. Patients taking ziconopeptide may experience cognitive and neuropsychiatric symptoms, decreased level of consciousness, and elevated serum creatine kinase levels. Furthermore, ziconopeptide may increase the risk of infections, including severe meningitis. Patients who discontinue opioids upon starting ziconopeptide are advised to gradually reduce the dose.

C102H172N36O32S7

2639.13408

2637.098

107452-89-1

Ziconotide acetate;914454-03-8;Ziconotide TFA

16135415

Typically exists as solid at room temperature

1.6±0.1 g/cm3

1.710

-17.05

1310.94

42

46

40

177

5480

22

NCCCCC1NC(=O)CNC(=O)C(CCCCN)NC(=O)C(N)CSSCC2C(NC(C(NCC(NC(C(NC3C(NC(C(NC(C(NCC(NC(C(NC(C(=O)N)CSSCC(C(N2)=O)NC(=O)C(CC(=O)O)NC(=O)C(CC2=CC=C(O)C=C2)NC(=O)C(CCSC)NC(=O)C(CC(C)C)NC(=O)C(CCCNC(=N)N)NC(=O)C(CO)NC(=O)C(CSSC3)NC(=O)C(CCCCN)NC(=O)C(C)NC(=O)CNC1=O)=O)CCCCN)=O)=O)CO)=O)CCCNC(=N)N)=O)=O)CO)=O)=O)C(O)C)=O

BPKIMPVREBSLAJ-QTBYCLKRSA-N

InChI=1S/C102H172N36O32S7/c1-50(2)34-63-91(161)127-62(26-33-171-5)90(160)129-64(35-53-22-24-54(143)25-23-53)92(162)130-65(36-78(148)149)93(163)135-72-48-175-173-45-69(80(108)150)133-86(156)58(18-8-12-29-105)121-76(146)39-117-85(155)66(41-139)131-88(158)61(21-15-32-114-102(111)112)126-96(166)70-46-176-177-47-71(97(167)132-68(43-141)95(165)125-60(87(157)128-63)20-14-31-113-101(109)110)134-89(159)59(19-9-13-30-106)123-81(151)51(3)119-74(144)37-115-83(153)56(16-6-10-27-103)120-75(145)38-116-84(154)57(17-7-11-28-104)124-82(152)55(107)44-172-174-49-73(137-98(72)168)99(169)138-79(52(4)142)100(170)118-40-77(147)122-67(42-140)94(164)136-70/h22-25,50-52,55-73,79,139-143H,6-21,26-49,103-107H2,1-5H3,(H2,108,150)(H,115,153)(H,116,154)(H,117,155)(H,118,170)(H,119,144)(H,120,145)(H,121,146)(H,122,147)(H,123,151)(H,124,152)(H,125,165)(H,126,166)(H,127,161)(H,128,157)(H,129,160)(H,130,162)(H,131,158)(H,132,167)(H,133,156)(H,134,159)(H,135,163)(H,136,164)(H,137,168)(H,138,169)(H,148,149)(H4,109,110,113)(H4,111,112,114)/t51-,52+,55-,56-,57-,58-,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,71-,72-,73-,79-/m0/s1

2-[(1R,4S,7S,13S,16R,21R,24S,27S,30S,33S,36S,39S,42R,45S,48S,54S,60S,63R,68R,71S,77S)-63-amino-13,45,54,60-tetrakis(4-aminobutyl)-4,36-bis(3-carbamimidamidopropyl)-16-carbamoyl-71-[(1R)-1-hydroxyethyl]-7,39,77-tris(hydroxymethyl)-27-[(4-hydroxyphenyl)methyl]-48-methyl-33-(2-methylpropyl)-30-(2-methylsulfanylethyl)-2,5,8,11,14,23,26,29,32,35,38,41,44,47,50,53,56,59,62,69,72,75,78,85-tetracosaoxo-18,19,65,66,81,82-hexathia-3,6,9,12,15,22,25,28,31,34,37,40,43,46,49,52,55,58,61,70,73,76,79,84-tetracosazatricyclo[40.37.4.221,68]pentaoctacontan-24-yl]acetic acid

Zicontide Acetate

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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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。