Endogenous reverse transcriptase (RT), particularly that encoded by LINE-1 elements. [1]
Telomerase (via downregulation of hTERT promoter activity). [3]
P2X7 purinergic receptor (ATP-P2X7). [2]

In prostate cancer cell lines, abacavir (15 and 150 μM, 0-120 hours) slows cell growth, modifies LINE-1 mRNA expression, promotes senescence, and changes cell cycle progression [1]. Cell migration is greatly reduced and cell invasion is inhibited by abacavir (15 and 150 μM, 18 hours) [1]. Adipocyte apoptosis is induced by abacavir [4].

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ABC (15 and 150 µM) significantly reduced cell growth rate, migration, invasion, and induced senescence and cell death in PC3 and LNCaP prostate cancer cells. In non-transformed WI-38 fibroblasts, 15 µM ABC did not cause significant growth inhibition, and 150 µM ABC induced only 20% inhibition after 120 h. [1]
ABC treatment caused cell cycle arrest in PC3 and LNCaP cells. In PC3 cells, 150 µM ABC led to a strong S phase accumulation at 18 and 24 h (56.3% and 78.6%, respectively), followed by a G2/M increase at 96 and 120 h. In LNCaP cells, a predominant S phase accumulation (40.5-54.3% at 48-72 h) was observed. [1]
Senescence-associated β-galactosidase activity was significantly induced by ABC (150 µM) over 5 days, reaching about 80% and 50% positive cells in PC3 and LNCaP cells, respectively. [1]
Scanning electron microscopy revealed that ABC treatment (15 µM, 48 h) caused PC3 cells to flatten, hindered their division process, and led to loss of surface microvilli. Nuclear morphology analysis showed bilobate/enlarged nuclei and scattered, less compact nucleoli. [1]
ABC (15 and 150 µM, 18 h treatment) significantly reduced cell migration (p < 0.001) and invasion (only at the higher dose) in PC3 and LNCaP cells in a dose-dependent manner. [1]
Microarray analysis on PC3 cells showed that ABC (15 and 150 µM, 48 h treatment) induced specific and dose-dependent changes in gene expression involving multiple cellular pathways. More genes were differentially expressed at 150 µM (3246 vs. 192). IPA analysis revealed top biological functions affected included cell death, cell cycle, cell morphology, RNA post-transcriptional modification, gene expression, and DNA replication. [1]
ABC treatment (15 and 150 µM, 24-120 h) induced a dose- and time-dependent up-regulation of LINE-1 ORF1 and ORF2 mRNA expression levels in PC3 and LNCaP cells. [1]
In DAOY, MEB-Med8a, and D283-Med medulloblastoma cell lines, the combination of ABC with ionizing radiation (IR) and decitabine (DEC) significantly reduced clonogenic survival (up to 1500-fold). [3]
In a co-incubation model of human umbilical vein endothelial cells (HUVEC) and platelets, ABC (100 µM) significantly enhanced platelet-endothelial cell interactions. [2]
ABC (100 µM) treatment up-regulated P2X7 receptor mRNA and protein expression levels in HUVEC. [2]

Dose-dependently, abacavir (100 and 200 mg/kg, PO; 4 hours) increases thrombosis [2]. In mice with high-risk medulloblastoma, abacavir (50 mg/kg/d; intraperitoneal injection; 14 days) and decitabine (0.1 mg/kg/d) can increase survival rates [3].

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In a PC3 subcutaneous xenograft mouse model, ABC (administered orally by gavage at 100 or 200 mg/kg) inhibited tumor growth during the first 15 days of treatment, though rebound growth was observed later. [1]
In a subcutaneous PC3 xenograft model, ABC (200 mg/kg/day) did not show significant tumor growth inhibition compared to control and did not induce body weight loss or changes in general condition. [2]
In orthotopic PDX mouse models of SHH/TP53-mut and Group 3 medulloblastoma (MB), multimodal therapy combining radiation (RT), decitabine (DEC), and abacavir (ABC) (RT/DEC/ABC) significantly inhibited tumor growth and enhanced mouse survival. Median survival increased from 44 to 66 days (50% increase) in Group 3 and from 59 to 73 days (24% increase) in SHH/TP53-mut models. ABC alone (50 mg/kg/day) did not significantly prolong survival. [3]
In the SHH/TP53-mut orthotopic MB model, tumor growth measured by MRI and BLI was significantly retarded in the RT/DEC/ABC treatment group. [3]
In the SHH/TP53-mut orthotopic MB model, the tumor proliferation index (Ki-67 positive cells) was significantly reduced in the RT/DEC/ABC group (to 75.6% of control). [3]
In the SHH/TP53-mut orthotopic MB model, tumor vascularization (CD31 staining) was significantly reduced in the RT/DEC/ABC group (all vessels to 78.9% of control). [3]
In a cremasteric arterial thrombosis model in C57BL/6 mice, local (intrascrotal, 2.5-7.5 µg/mL) or oral (100-200 mg/kg, 4 h pretreatment) administration of ABC dose-dependently promoted FeCl3-induced arterial thrombus formation (shortened time to occlusion). [2]
The pro-thrombotic effect of ABC (5 µg/mL, i.s.) in the murine cremasteric thrombosis model was reversed by a P2X7 receptor antagonist (A804598) and was absent in P2X7 knockout (P2rx7 KO) mice. [2]
In HIV-infected patients, 48 weeks after switching from stavudine (d4T) to abacavir (ABC) or zidovudine (ZDV), median arm, leg, and trunk fat increased by 21%, 11%, and 16% respectively (by DEXA). This was accompanied by significant rebounds in mitochondrial DNA (mtDNA) levels in PBMC, muscle, and adipose tissue (mean increases of 369%, 141%, and 146%, respectively), and a significant reduction in adipocyte apoptosis. [4]

Endogenous Reverse Transcriptase (RT) Activity Assay: MS2 phage RNA was used as a template with an MS2 reverse primer. Cell-free extracts (24 µg total protein) from PC3, LNCaP, or WI-38 cells were used as the RT source instead of commercial RT. Reactions were incubated at 55°C for 1 h, followed by 5 min at 85°C. E. coli RNaseH was added and incubated at 37°C for 20 min. The product was PCR-amplified using MS2 forward and reverse primers (94°C for 2 min; 30 cycles of 94°C for 30 s, 58°C for 30 s, 72°C for 30 s), yielding a 112-bp DNA fragment. PCR products were analyzed by 1.5% agarose gel electrophoresis. RT activity was detected in PC3 and LNCaP cells but was undetectable in WI-38 cells. [1]
Mitochondrial Electron Transport Chain (ETC) Complex Activity Assay: Assays were performed on homogenates prepared from patient skeletal muscle biopsies. Activities measured included NADH cytochrome c reductase (complexes I & III), NADH ferricyanide reductase (complex I), succinate cytochrome c reductase (complexes II & III), succinate dehydrogenase, decylubiquinol cytochrome c reductase (complex III), cytochrome c oxidase (complex IV), and citrate synthase (a marker of mitochondrial mass). At baseline (on d4T), activities of complexes I-IV ranged from 48% to 85% of control levels. After 48 weeks of switching from d4T to ABC or ZDV, NADH cytochrome c reductase activity significantly improved from 0.6 ± 0.5 to 0.9 ± 0.6 (unit: nmol/min/g wet weight). [4]

Cell proliferation assay [1]
Cell Types: PC3, LNCaP and WI-38
Tested Concentrations: 15 and 150 μM
Incubation Duration: 0, 24, 48, 72 and 96 h
Experimental Results: Dose-dependent growth inhibition was shown for PC3 and LNCaP.

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Cell cycle analysis [1]
Cell Types: PC3 and LNCaP
Tested Concentrations: 150 μM
Incubation Duration: 0, 18, 24, 48, 72, 96 and 120 h
Experimental Results: Caused a large accumulation of S phase cells in PC3 and LNCaP cells, and in An increase in G2/M phase was observed in PC3 cells.

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Cell migration assay[1]
Cell Types: PC3 and LNCaP
Tested Concentrations: 15 and 150 μM
Incubation Duration: 18 hrs (hours)
Experimental Results: Significant reduction in cell migration.

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Cell invasion assay[1]
Cell Types: PC3 and LNCaP
Tested Concentrations: 15 and 150 μM
Incubation Duration: 18 hrs (hours)
Experimental Results: Significant inhibition of cell invasion.

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Cell Proliferation Assay: PC3, LNCaP, and WI-38 cells were seeded at 20,000 per well in 12-well plates, cultured for 24 h, then treated with ABC at 15 or 150 µM. At 0, 24, 48, 72, and 96 h, the number of trypan blue-excluding cells was counted. Experiments were performed three times in triplicate. [1]
Cell Cycle Analysis: Treated and untreated cells were harvested, washed with PBS, and stained using a DNA staining kit. DNA content was then analyzed by flow cytometry. [1]
Senescence Determination: The percentage of senescent cells was measured by detecting β-galactosidase activity at pH 6.0 using a commercial kit. Data were quantified from >500 cell counts in three independent experiments. [1]
Cell Migration and Invasion Assays: Transwell chambers with 8.0 µm pore filters were used. Cells were suspended in RPMI at 1x10^6 cells/mL and added to the upper chamber. RPMI with 10% FBS was added to the lower chamber. For the invasion assay, filters were pre-coated with Matrigel. Cells were incubated at 37°C for 18 h. Afterwards, cells on the inner side of the filter were removed with a swab, and the outer side was stained with crystal violet. The percent area occupied by migrated or invaded cells was analyzed. [1]
qRT-PCR for LINE-1 mRNA Expression: Total RNA was isolated from cells treated with ABC. RNA was DNase-treated. cDNA was synthesized. Relative quantification PCR was performed using TaqMan chemistry with custom primers and FAM-MGB probes for LINE-1 ORF1 and ORF2. GAPDH was used as an endogenous control. Gene expression differences were calculated by the 2^-ΔΔCt method. [1]
Apoptosis Assay (TUNEL): Terminal deoxynucleotide transferase dUTP-digoxigenin nick-end labeling (TUNEL) was performed on fixed sections of subcutaneous adipose tissue from study subjects. Histology was assessed by a pathologist blinded to sample details. Apoptosis was graded from 0 (no TUNEL-positive cells) to 3 (most adipocytes TUNEL positive). [4]

Animal/Disease Models: Male mouse (9 weeks old, 22-30 g) - wild type (WT) C57BL/6 or homozygous knockout (P2rx7 KO, B6.129P2-P2rx7tm1Gab/J) [2]
Doses: 2.5, 5 and 7.5 μg/mL, 100 μL, or 100 and 200 mg/kg
Route of Administration: Intrascrotal or oral administration over 4 hrs (hrs (hours))
Experimental Results: Dose-dependent promotion of thrombosis.

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Animal/Disease Models: NSGTM mice, patient-derived xenograft (PDX) cells of non-WNT/non-SHH, group 3 and SHH/TP53 mutant medulloblastoma [3]
Doses: 50 mg/kg/d, 0.1 mg/kg /d Decitabine
Route of Administration: intraperitoneal (ip) injection, one time/day for 14 days
Experimental Results: Inhibited tumor growth and improved mouse survival.

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PC3 Subcutaneous Xenograft Model: PC3 cells (5x10^6) were injected subcutaneously into the flank of nude mice. When tumors reached ~100 mm³, mice were randomized. ABC was administered orally by gavage at 100 or 200 mg/kg once daily for 15 days. Tumor volume and body weight were measured twice weekly. [1]
Orthotopic Medulloblastoma PDX Model: Approximately 8x10^4 patient-derived medulloblastoma (Group 3 or SHH/TP53-mut) cells were stereotactically injected into the cerebellum of NSG mice. Tumor growth was monitored by bioluminescence imaging (BLI) and/or magnetic resonance imaging (MRI). Therapy started upon first BLI signal (day 21 for Group 3, day 7 for SHH/TP53-mut). Treatment groups included: sham (control), RT (single dose whole-brain irradiation: 2 Gy for Group 3, 4 Gy for SHH/TP53-mut), DEC (0.1 mg/kg/day, i.p.), ABC (50 mg/kg/day, i.p.), and combinations. Drugs were administered daily from day 1 to 14. RT was given on day 8. Primary endpoints were mouse survival (time from implantation to euthanasia) and tumor growth (by BLI and MRI). [3]
Cremasteric Arterial Thrombosis Model: Male 9-week-old C57BL/6 wild-type or P2rx7 KO mice were anesthetized with xylazine (10 mg/kg) and ketamine (100 mg/kg) i.p. The cremaster muscle was exteriorized and superfused with bicarbonate-buffered saline. Single unbranched cremasteric arterioles (diameter 20-35 µm) were visualized. Thrombosis was induced by superfusion with 25 mM FeCl3. Time to cessation of blood flow (occlusion time) was recorded. Centerline red blood cell velocity (Vrbc) was measured before and after FeCl3 challenge. ABC was administered either intrascrotally (2.5-7.5 µg/mL) or orally (100-200 mg/kg) 4 hours before FeCl3 challenge. Antagonists (A804598, A317491) were given i.p. 30 min before ABC. [2]
Clinical NRTI Switch Study (Substudy of TARHEEL): 16 HIV-infected patients on stavudine (d4T) for >3 years with lipoatrophy and/or hyperlactatemia switched d4T to abacavir (ABC) or zidovudine (ZDV) in their antiretroviral regimen. At baseline (before switch) and week 48, the following were performed: DEXA scans for body fat changes; blood draw for PBMC isolation; fat and muscle biopsies from the lateral thigh. These samples were analyzed for mtDNA levels (PBMC, fat, muscle), muscle mitochondrial ETC activities, adipocyte apoptosis (TUNEL), and cytokine mRNA expression in fat. [4]

Absorption, Distribution and Excretion
After oral administration, it is rapidly and extensively distributed (tablet bioavailability is 83%). Following twice-daily administration of 300 mg tablets, the peak plasma concentration (Cmax) was 3.0 ± 0.89 mcg/mL, and the area under the curve (AUC 0–12 hours) was 6.02 ± 1.73 mcg•hr/mL. Following administration of a 600 mg dose of SUP14C-abacavir, the elimination of abacavir was quantitatively analyzed by a mass balance study: 99% of the radioactive material was recovered, 1.2% was excreted in the urine as abacavir, 30% as a 5′-carboxylic acid metabolite, 36% as a 5′-glucuronide metabolite, and 15% as unidentified minor metabolites in the urine. Fecal excretion accounted for 16% of the total dose. Abacavir is excreted unchanged via the kidneys, with limited excretion pathways in the human body.
0.86 ± 0.15 L/kg [intravenous administration]
0.80 ± 0.24 L/hr/kg [single intravenous dose of 150 mg for asymptomatic HIV-1 infected adults]
Metabolism/Metabolites
Primarily metabolized in the liver by alcohol dehydrogenases and glucuronyl transferases to 5'-carboxylic acid metabolites and 5'-glucuronide metabolites. These metabolites do not possess antiviral activity. Abacavir is hardly metabolized by cytochrome P450 enzymes.
Biological half-life
1.54 ± 0.63 hours

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Plasma concentrations of ABC in mice 4 hours after oral administration of 100 mg/kg and 200 mg/kg were 5.3 ± 0.8 µg/mL and 16.2 ± 1.9 µg/mL, respectively. [2]

Hepatotoxicity
Up to 6% of patients taking abacavir may experience serum transaminase levels exceeding 5 times the upper limit of normal. These elevations are usually mild and transient, requiring no dose adjustment. Clinically significant hepatotoxicity is rare, but isolated cases have been reported (usually without jaundice). Liver injury typically occurs against the backdrop of abacavir hypersensitivity syndrome and may be masked by allergic symptoms such as fever, rash, and fatigue. It usually appears within 1 to 3 months after starting abacavir. Serum enzyme profiles can be hepatocellular or cholestatic. Patients usually recover rapidly within 4 weeks after discontinuation of the drug. Probability score: C (likely the cause of clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Abacavir is present in small amounts in breast milk. Information on the safety of using this drug during lactation is very limited. Achieving and maintaining viral suppression through antiretroviral therapy can reduce the risk of breast milk transmission to below 1%, but not zero. For HIV-infected individuals receiving antiretroviral therapy with persistently undetectable viral load, breastfeeding should be supported if chosen. If viral load is not suppressed, pasteurized donated breast milk or formula is recommended.
◉ Effects on Breastfed Infants
An HIV-positive mother took a once-daily combination tablet (Triumeq) containing 50 mg dolutegravir, 600 mg abacavir sulfate, and 300 mg lamivudine. Her infant was exclusively breastfed for approximately 30 weeks, followed by partial breastfeeding for approximately 20 weeks. No significant side effects were observed.
◉ Effects on Lactation and Breast Milk
Gynecomastia has been reported in men receiving highly active antiretroviral therapy. Gynecomastia is initially unilateral, but approximately half of cases develop into bilateral gynecomastia. No changes in serum prolactin levels were observed, and it usually resolves spontaneously within one year even with continued medication. Some case reports and in vitro studies suggest that protease inhibitors may cause hyperprolactinemia and galactorrhea in some male patients, but this conclusion remains controversial. The implications of these findings for lactating women are unclear. Prolactin levels in established lactating mothers may not affect their ability to breastfeed. Protein binding is moderate (approximately 50%). Abacavir's binding to plasma proteins is concentration-independent.

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In non-transformed WI-38 fibroblasts, 15 µM ABC did not cause significant growth inhibition, while 150 µM induced only 20% inhibition after 120 h, suggesting low toxicity to normal cells. [1]
In the SHH/TP53-mut orthotopic MB model, no overt adverse effects (e.g., weight loss, poor general condition) were observed in mice receiving the RT/DEC/ABC multimodal therapy. Liver biopsies showed no organ toxicity. [3]
In C57BL/6 mice, single-dose whole-brain irradiation (WBI) at 5 or 10 Gy caused diminished general condition and weight loss, while 2-4 Gy did not. Decitabine (DEC) at higher doses (0.5, 1 mg/kg/day) caused poor condition and weight loss, whereas 0.1 mg/kg/day was well tolerated. Abacavir (ABC) caused no adverse effects at the doses tested (10, 20, 50 mg/kg/day). [3]
In HIV-infected patients, switching from d4T to ABC or ZDV for 48 weeks resulted in a significant decrease in serum lactate levels (median change -0.40 mmol/L, p=0.012). No serious adverse events resulted from the biopsy procedures; only self-limited pain or small painless seromas at the incision site occurred in some subjects. [4]
In HIV-infected patients, adipocyte apoptosis levels were significantly higher at baseline (on d4T) compared to HIV-negative controls. After 48 weeks of switching from d4T to ABC or ZDV, adipocyte apoptosis levels were significantly reduced. [4]

[1]. The reverse transcription inhibitor abacavir shows anticancer activity in prostate cancer cell lines. PLoS One. 2010 Dec 3;5(12):e14221.

[2]. Abacavir Induces Arterial Thrombosis in a Murine Model. J Infect Dis. 2018 Jun 20;218(2):228-233.

[3]. Enhanced Survival of High-Risk Medulloblastoma-Bearing Mice after Multimodal Treatment with Radiotherapy, Decitabine, and Abacavir. Int J Mol Sci. 2022 Mar 30;23(7):3815.

[4]. Improvements in lipoatrophy, mitochondrial DNA levels and fat apoptosis after replacing stavudine with abacavir or zidovudine. AIDS. 2005 Jan 3;19(1):15-23.

Abacavir is a 2,6-diaminopurine, chemically named (1S)-cyclopent-2-en-1-ylmethanol, where the pro-R hydrogen at the 4-position is replaced by a 2-amino-6-(cyclopropylamino)-9H-purine-9-yl group. It is a nucleoside reverse transcriptase inhibitor (NRTI) with anti-HIV activity and is often used in combination with other antiretroviral drugs for the treatment of HIV infection (especially in its sulfate form). It is an HIV-1 reverse transcriptase inhibitor, an antiviral drug, and also a drug allergen. Abacavir (trade name: Ziagen) is a prescription drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of HIV infection in adults, children, and infants. Abacavir is often used in combination with other anti-HIV drugs. Abacavir (ABC) is a potent nucleoside analog reverse transcriptase inhibitor (NRTI) used to treat HIV infection and AIDS. Chemically, it is a synthetic carbocyclic nucleoside, an enantiomer with an absolute 1S,4R configuration on the cyclopentene ring. In vivo, abacavir sulfate dissociates into the free base abacavir. Abacavir is a human immunodeficiency virus nucleoside analog reverse transcriptase inhibitor. Its mechanism of action is as a nucleoside reverse transcriptase inhibitor and a cytochrome P450 1A1 inhibitor. Abacavir sulfate is a nucleoside analog and reverse transcriptase inhibitor used in combination with other drugs to treat human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS). Abacavir is a rare cause of clinically significant drug-induced liver injury. Abacavir is a nucleoside reverse transcriptase inhibitor, an analog of guanosine. This drug can reduce HIV viral load, delay or prevent damage to the immune system, and reduce the risk of developing AIDS.

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Drug Indications
Abacavir is used in combination with other antiretroviral drugs to treat HIV-1 infection.
It is used in combination with dolutegravir and lamivudine to treat HIV-1 infection in adults and children weighing ≥10 kg.
FDA Label
Ziagen is indicated for use as an antiretroviral combination therapy in adults, adolescents, and children for the treatment of human immunodeficiency virus (HIV) infection. The efficacy of Ziagen is primarily based on studies in treatment-naïve adult patients receiving combination therapy using a twice-daily dosing regimen. All HIV-infected individuals, regardless of race, should be screened for HLA-B5701 allele carriage before initiating abacavir treatment. Abacavir is contraindicated in patients known to carry the HLA-B5701 allele.

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Mechanism of Action
Abacavir is a carbocyclic synthetic nucleoside analog and an antiviral drug. Intracellularly, abacavir is converted by cellular enzymes to its active metabolite, carbovir triphosphate, an analog of deoxyguanosine-5'-triphosphate (dGTP). Carbovir triphosphate inhibits HIV-1 reverse transcriptase (RT) activity by competing with the natural substrate dGTP and by incorporating it into viral DNA. Viral DNA growth terminates because the incorporated nucleotide lacks a 3'-OH group, which is essential for the formation of a 5' to 3' phosphodiester bond, crucial for DNA chain elongation.

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Mechanism of Action: ABC is a nucleoside reverse transcriptase inhibitor (NRTI) that is converted by cellular enzymes to its active carbovir triphosphate form, an analogue of dGTP. It inhibits reverse transcription by being incorporated into the newly synthesized viral DNA chain, preventing further elongation. ABC shows very low affinity for cellular DNA polymerases compared to other NRTIs. [1]
Clinical Association/Controversy: ABC is widely used in HIV therapy. Since 2005, clinical studies (notably the D:A:D study) have associated current or recent (≤6 months) ABC use with a two-fold increased risk of myocardial infarction (MI). This association remains controversial as other studies have not confirmed the risk. Despite this, major clinical guidelines recommend caution when prescribing ABC to patients at risk of cardiovascular disease. [2]
Safety Warning: The pro-thrombotic effect of ABC in the murine arterial thrombosis model was similar to that of recognized vascular-damaging agents like rofecoxib and diclofenac, providing a potential pharmacological explanation for the clinical cardiovascular risk signals. [2]

C14H18N6O

286.34

286.154

136470-78-5

Abacavir sulfate;188062-50-2;Abacavir monosulfate;216699-07-9;Abacavir hydrochloride;136777-48-5;Abacavir-d4;1260619-56-4;rel-Abacavir-d4;1217731-56-0

441300

White to off-white solid powder

1.7±0.1 g/cm3

636.0±65.0 °C at 760 mmHg

161 °C(dec.)

338.4±34.3 °C

0.0±2.0 mmHg at 25°C

1.864

0.72

3

6

4

21

414

2

C1CC1NC2=C3C(=NC(=N2)N)N(C=N3)[C@@H]4C[C@@H](C=C4)CO

MCGSCOLBFJQGHM-SCZZXKLOSA-N

InChI=1S/C14H18N6O/c15-14-18-12(17-9-2-3-9)11-13(19-14)20(7-16-11)10-4-1-8(5-10)6-21/h1,4,7-10,21H,2-3,5-6H2,(H3,15,17,18,19)/t8-,10+/m1/s1

[(1S,4R)-4-[2-amino-6-(cyclopropylamino)purin-9-yl]cyclopent-2-en-1-yl]methanol

EpzicomABC, Ziagen

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)

DMSO : ~100 mg/mL (~349.25 mM)
H2O : ~2 mg/mL (~6.98 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 3.33 mg/mL (11.63 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with heating and sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)