Pentoxifylline: Tumor Necrosis Factor-α (TNF-α) (inhibitory activity), Nuclear Factor-kappa B (NF-κB) (suppressive effect), Phosphodiesterase 4 (PDE4) (weak inhibition) [1]
Pentoxifylline: Acts on pathways regulating red blood cell deformability, blood viscosity, and platelet aggregation [2]
Pentoxifylline: Extracellular Signal-Regulated Kinase 1/2 (ERK1/2) and Protein Kinase B (AKT) (activating effect), Mammalian Target of Rapamycin (mTOR) [3]

Pentoxifylline suppresses cell growth in a dose-dependent manner (0.1–50 mM; 24-48 hours) [3]. In MDA-MB-231 cells, pentoxifylline (0.5 mM; 12-36 hours) decreases autophagy and promotes apoptosis [3]. In MDA-MB-231 cells, pentoxifylline (0.5 mM; 12-36 hours) promotes autophagy [3]. The G0/G1 phase of the cell cycle is blocked by pentoxifylline (0.5 mM; 24-48 hours) [3]. Elevated LC3-II/LC3 ratio is brought on by pentoxifylline [3].

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1. In human leukocytes, Pentoxifylline concentration-dependently inhibited the production of pro-inflammatory cytokines TNF-α and IL-1β induced by bacterial stimulation, while upregulating the expression of anti-inflammatory cytokine IL-10 [1]
2. Pentoxifylline increased red blood cell deformability in vitro, reduced whole blood viscosity by decreasing erythrocyte aggregation, and inhibited platelet aggregation induced by ADP and collagen (inhibition rate not specified) [2]
3. In triple-negative MDA-MB-231 breast cancer cells, Pentoxifylline (0.5 mM) alone inhibited cell proliferation by 42% after 48-hour treatment, induced apoptosis in 25% of cells and autophagy in 25% of cells; when combined with simvastatin (0.5 μM), the proliferation inhibition rate reached 80%, apoptosis rate increased to >65%, and autophagy rate decreased to <13% [3]
4. Co-treatment with Pentoxifylline (0.5 mM) and simvastatin (0.5 μM) caused G0/G1 cell cycle arrest in 78% of MDA-MB-231 cells, and the colony-forming ability of the cells was reduced to 38±5% (vs. 115±5% with Pentoxifylline alone) [3]
5. Pentoxifylline (0.5 mM) activated the phosphorylation of ERK1/2 and AKT in MDA-MB-231 cells, suppressed the NF-κB signaling pathway, and had no significant effect on mTOR phosphorylation; the combined treatment also increased reactive oxygen species (ROS) levels and caspase 3 activity in the cells [3]

In rats exposed to transitory global ischemia, pentoxifylline (200 mg/kg; i.p.) exerts a protective effect and lessens cognitive damage [4].

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1. Pentoxifylline showed therapeutic efficacy in the treatment of dermatological diseases such as leg ulcers, psoriasis, and scleroderma, either as a primary or adjuvant drug [1]
2. In patients with peripheral vascular disease, oral administration of Pentoxifylline (600–1200 mg/day for at least 6 weeks) improved walking distance by approximately 100%, relieved rest pain and paresthesia of the lower limbs, increased muscle blood flow, and promoted the healing of leg ulcers, with an effective rate of 60–100% [2]
3. In patients with cerebrovascular disorders, Pentoxifylline (600–1200 mg/day, 300–600 mg/day in Japan) achieved marked clinical improvement in about 85% of patients, increased cerebral blood flow (especially in ischemic areas), and improved neuromotor deficits, speech disorders and subjective symptoms [2]
4. Pentoxifylline exhibited better therapeutic effects than placebo, nylidrin, adenosine, and naftidrofuryl in the treatment of peripheral vascular disease, and was superior to co-dergocrine mesylate, adenosine and pyrithioxine in chronic cerebrovascular disease [2]
5. In a rat model of transient global cerebral ischemia, intraperitoneal injection of Pentoxifylline (200 mg/kg, administered 1 hour before and 3 hours after ischemia) significantly improved hippocampus-dependent spatial memory in the Morris Water Maze test, reduced ischemia-induced cognitive impairment, and the number of pyramidal cells in the hippocampal CA1 region was not significantly different from the control group [4]

1. Cytokine production assay in human leukocytes: Human leukocytes were isolated from peripheral blood and incubated with bacterial stimulants and different concentrations of Pentoxifylline in a suitable culture medium for a preset period. After incubation, the culture supernatant was collected, and the concentrations of TNF-α, IL-1β and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA) to calculate the inhibition or promotion rate of cytokine production [1]
2. Caspase 3 activity assay: MDA-MB-231 cells were treated with Pentoxifylline alone or in combination with simvastatin for 48 hours, then cell lysates were prepared by lysing the cells with a lysis buffer. Caspase 3 activity was measured using a colorimetric substrate kit, and the absorbance value at 405 nm was detected with a microplate reader to reflect the relative activity of caspase 3 [3]
3. Reactive oxygen species (ROS) detection assay: MDA-MB-231 cells were seeded in culture plates and loaded with a fluorescent probe specific for ROS. After loading, the cells were treated with Pentoxifylline and simvastatin for a specific time, and the fluorescence intensity of the cells was detected by flow cytometry to quantify the intracellular ROS level [3]

Cell proliferation assay[3]
Cell Types: MDA-MB-231 Cell
Tested Concentrations: 0.1 mM, 1 mM, 5 mM, 10 mM, 50 mM
Incubation Duration: 24 hrs (hours), 48 hrs (hours)
Experimental Results: Inhibition of cell proliferation in a dose-dependent manner.

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Apoptosis analysis[3]
Cell Types: MDA-MB-231 Cell
Tested Concentrations: 0.5 mM
Incubation Duration: 12 hrs (hours), 24 hrs (hours), 36 hrs (hours)
Experimental Results: Induction of apoptosis.

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Autophagy assay [3]
Cell Types: MDA-MB-231 Cell
Tested Concentrations: 0.5 mM
Incubation Duration: 24 hrs (hours), 48 hrs (hours)
Experimental Results: Approximately 20-28% of autophagy was induced.

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Cell cycle analysis [3]
Cell Types: MDA-MB-231 Cell
Tested Concentrations: 0.5 mM
Incubation Duration: 24 hrs (hours), 48 hrs (hours)
Experimental Results: Induced G0/G1 phase arrest.

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Western Blot Analysis[3]
Cell Types: MDA-MB-231 Cell
Tested Concentrations: 0.5 mM
Incubation Duration: 24 hrs (hours), 48 hrs (hours)
Experimental Results: Induction of high LC3-II/LC3 ratio.

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1. MTT cell proliferation assay: MDA-MB-231 cells were seeded in 96-well plates at a density of 5×10³ cells per well and cultured overnight. The cells were then treated with Pentoxifylline (0.5 mM) alone or in combination with simvastatin (0.5 μM) for 48 hours. MTT solution was added to each well and incubated for 4 hours, after which the supernatant was discarded and dimethyl sulfoxide (DMSO) was added to dissolve the formazan crystals. The absorbance at 570 nm was measured with a microplate reader, and the cell proliferation inhibition rate was calculated based on the absorbance values of the treatment groups and the control group [3]
2. Colony-forming assay: MDA-MB-231 cells were seeded in 6-well plates at a low density (200 cells per well) and cultured overnight. The cells were treated with Pentoxifylline and simvastatin, and the culture medium was refreshed every 3 days. After 14 days of culture, the colonies were fixed with fixative solution and stained with crystal violet. The number of colonies containing more than 50 cells was counted, and the colony-forming efficiency was calculated [3]
3. Apoptosis detection by Annexin V/PI staining: MDA-MB-231 cells were treated with drugs for 48 hours, then harvested and washed with phosphate-buffered saline (PBS). The cells were stained with Annexin V-FITC and propidium iodide (PI) according to the staining protocol, and incubated in the dark for 15 minutes. The apoptotic rate was analyzed by flow cytometry, with early apoptosis defined as Annexin V-positive/PI-negative and late apoptosis/necrosis defined as Annexin V-positive/PI-positive [3]
4. Cell cycle analysis: MDA-MB-231 cells were treated with drugs for 48 hours, harvested and fixed with 70% cold ethanol at 4°C overnight. The fixed cells were washed with PBS, stained with PI solution containing RNase, and incubated in the dark for 30 minutes. The cell cycle distribution (G0/G1, S, G2/M phases) was detected by flow cytometry, and the percentage of cells in each phase was calculated [3]
5. Western blot analysis: MDA-MB-231 cells were treated with drugs for 48 hours, then lysed to extract total cellular protein. The protein samples were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and transferred to a polyvinylidene fluoride (PVDF) membrane. The membrane was blocked with blocking buffer and incubated with primary antibodies against ERK1/2, phosphorylated ERK1/2 (p-ERK1/2), AKT, phosphorylated AKT (p-AKT), mTOR, phosphorylated mTOR (p-mTOR) and NF-κB, followed by incubation with secondary antibodies. The protein bands were visualized by a chemiluminescent substrate, and the band intensity was quantified by densitometry and normalized to the internal reference protein [3]
6. DNA fragmentation assay: Genomic DNA was extracted from MDA-MB-231 cells treated with Pentoxifylline and simvastatin using a DNA extraction kit. The extracted DNA was separated by 1.5% agarose gel electrophoresis, stained with ethidium bromide, and the DNA fragmentation pattern (ladder-like bands) was observed under ultraviolet light to confirm apoptosis [3]
7. Autophagic vesicle detection: MDA-MB-231 cells were treated with drugs for 48 hours, then stained with a fluorescent dye that specifically labels autophagic vesicles. The cells were observed under a fluorescence microscope, and the number of autophagic vesicles per cell was counted; alternatively, the fluorescence intensity was detected by flow cytometry to quantify the level of autophagy [3]

Animal/Disease Models: Adult male Wistar rats, 12-13 weeks old (250-300 g) [4]
Doses: 200 mg/kg
Route of Administration: intraperitoneal (ip) injection, 1 hour before ischemia and 3 hrs (hrs (hours)) after ischemia.
Experimental Results: Significant Improves spatial memory and memory abilities. The effect was Dramatically different from that of the sham operation group and the vehicle group.

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1. Rat model of transient global cerebral ischemia: Thirty-two male Wistar rats (250–300 g) were randomly divided into four groups: control group, sham-operated group, vehicle group, and Pentoxifylline-treated group. Pentoxifylline was dissolved in a suitable vehicle , and administered intraperitoneally at a dose of 200 mg/kg (1 hour before ischemia and 3 hours after ischemia). Transient global cerebral ischemia was induced by bilateral common carotid artery occlusion for 20 minutes, followed by reperfusion. After reperfusion, the Morris Water Maze test was performed to evaluate spatial memory: the escape latency to find the hidden platform and the distance moved were recorded during the training phase, and the number of platform crossings and the time spent in the target quadrant were recorded during the probe trial. After the behavioral test, the rats were sacrificed, and brain sections were prepared and stained with Nissl staining to count the number of pyramidal cells in the hippocampal CA1 region [4]
2. Clinical trial for peripheral vascular disease: Patients with peripheral vascular disease were treated with oral controlled-release Pentoxifylline tablets at a dose of 600–1200 mg/day for at least 6 weeks. Clinical parameters including maximum walking distance, claudication distance, rest pain score, paresthesia symptoms, muscle blood flow (measured by Doppler ultrasound), and leg ulcer healing status were assessed at 2-week intervals during the treatment period [2]
3. Clinical trial for cerebrovascular disease: Patients with chronic cerebrovascular disorders received oral Pentoxifylline at a dose of 600–1200 mg/day (300–600 mg/day in Japan) for a long-term period (≥3 months). Cerebral blood flow was measured by single-photon emission computed tomography (SPECT) or computed tomography (CT) perfusion imaging, and neurological function was evaluated using a standardized neurological deficit score, including assessments of motor function, speech ability, and subjective symptoms such as dizziness and headache [2]

Absorption, Distribution and Excretion
Orally administered pentoxifylline (PTX) is almost completely absorbed, but its bioavailability is low, only 20-30%, due to extensive first-pass metabolism. Three of the seven known metabolites, M1, M4, and M5, are present in plasma and appear shortly after administration. In healthy men, a single oral dose of 100, 200, and 400 mg of pentoxifylline resulted in a mean time to peak concentration (tmax) of 0.29-0.41 hours, a mean plasma concentration (Cmax) of 272-1607 ng/mL, and a mean AUC0-∞ of 193-1229 ngh/mL; the corresponding ranges for metabolites 1, 4, and 5 were 0.72-1.15, 114-2753, and 189-7057, respectively. Following a single 400 mg extended-release tablet, the time to peak concentration (tmax) was prolonged to 2.08 ± 1.16 h, and the peak plasma concentration (Cmax) decreased to 55.33 ± 22.04 ng/mL, while the AUC0-t value was close to normal at 516 ± 165 ngh/mL; all these parameters were elevated in patients with cirrhosis. Smoking was associated with decreased Cmax and steady-state AUC of metabolite M1, but had no significant effect on the pharmacokinetic parameters of pentoxifylline or other assay metabolites. Renal impairment increased the mean Cmax, AUC, and their ratio to the parent compound AUC of metabolites M4 and M5, but had no significant effect on the pharmacokinetics of pentoxifylline or M1. Finally, similar to patients with cirrhosis, patients with varying degrees of chronic heart failure showed elevated Cmax and tmax of pentoxifylline and its metabolites. Overall, the plasma concentrations of metabolites M1 and M5 were approximately five and eight times higher than those of PTX, respectively. The pharmacokinetics of PTX and M1 are approximately dose-dependent, while those of M5 are not. Taking PTX with food before administration delays the time to peak plasma concentration but does not affect overall absorption. Extended-release PTX formulations can prolong the time to peak concentration to two to four hours and also help improve the time-varying fluctuations in plasma concentrations. Pentoxoborobromine is almost entirely excreted in the urine, primarily as M5, which accounts for 57% to 65% of the administered dose. A small amount of M4 is recovered, while the recovery of M1 and the parent compound is less than 1%. Fecal administration accounts for less than 4% of the administered dose. The volume of distribution after a single intravenous injection of 100 mg pentoxoborobromine in healthy subjects is 4.15 ± 0.85. The clearance rate of a single intravenous infusion of 100 mg pentoxifylline in healthy subjects was 3.62 ± 0.75 L/h/kg, while the clearance rate decreased to 1.44 ± 0.46 L/h/kg in patients with cirrhosis. Another study showed that the apparent clearance rates (median and range) of intravenous injections of 300 mg or 600 mg pentoxifylline were 4.2 (2.8–6.3) L/min and 4.1 (2.3–4.6) L/min, respectively. It is noteworthy that the true clearance rate of pentoxifylline may be higher than the measured values because the extrahepatic metabolism of the parent compound and metabolite 1 is reversible. The metabolic mechanism of pentoxifylline (PTX) is not fully understood. Seven metabolites (M1 to M7) are currently known, but only M1, M4, and M5 are detectable in plasma, with the overall pattern being M5 > M1 > PTX > M4. Since the apparent clearance of PTX is higher than that of hepatic blood flow, and the AUC ratio of M1 to PTX does not differ significantly in patients with cirrhosis, erythrocytes can be identified as the primary site of PTX-M1 interconversion. However, this reaction can also occur in the liver. Paclitaxel (PTX) is reduced in a NADPH-dependent manner by an unknown carbonyl reductase to lisoferrine ((R)-M1 enantiomer) or (S)-M1; this reaction is stereoselective, generating only (S)-M1 in the hepatic cytoplasm and 85% (S)-M1 in the liver microsomes, with an R:S-M1 ratio of 0.010–0.025 after intravenous or oral administration in humans. Although both (R)-M1 and (S)-M1 can be oxidized back to PTX, (R)-M1 can also generate M2 and M3 in the liver microsomes. In vitro studies have shown that CYP1A2 is at least partially involved in the reduction of lisoferrine ((R)-M1) back to PTX. Unlike the reversible redox reactions of PTX and its M1 metabolites, M4 and M5 are generated via the irreversible oxidation of PTX in the liver. Studies simulating the PTX-ciprofloxacin drug response in mice have shown that CYP1A2 is responsible for converting PTX to M6 and M1 to M7, both generated via 7-position demethylation. Typically, metabolites M2, M3, and M6 are produced in very low amounts in mammals. Pentoxobocytobacter is a known human metabolite of lisoferrine. Overall, the elimination half-life of pentoxobocytobacter is 0.39 to 0.84 hours, while the elimination half-life of its major metabolite is 0.96 to 1.61 hours.

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1. Absorption: After oral administration, pentoxifylline is rapidly absorbed in the human body, and the peak plasma concentration (Cmax) is reached within 1-2 hours; due to extensive first-pass metabolism in the liver, the oral bioavailability is only about 10-20% [2]
2. Distribution: Pentoxifylline has a plasma protein binding rate of about 98% in the human body; it is well distributed in various tissues, and its concentration is higher in ischemic brain regions and peripheral vascular tissues compared with normal tissues [2]
3. Metabolism: Pentoxifylline is mainly metabolized in the liver by cytochrome P450 (CYP) enzymes, producing two main active metabolites: 1-(5-hydroxyhexyl)-3,7-dimethylxanthine and 1-(3-carboxypropyl)-3,7-dimethylxanthine [2]
4. Elimination: The terminal half-life (t1/2) of pentoxifylline in the human body is about 0.5–1.5 hours; about 90% of the metabolites are eliminated within 24 hours. It is excreted by the kidneys within hours, with only a small amount of the original drug being excreted unchanged [2]
5. Pharmacokinetic parameters (human, oral 600 mg): Cmax ≈ 1 μg/mL, Tmax = 1–2 hours, area under the plasma concentration-time curve (AUC0-∞) ≈ 2 μg·h/mL [2]

Hepatotoxicity
Long-term use of pentoxifylline is not associated with elevated serum enzyme levels, although the rigor of liver function tests in patients taking this drug is not always clear. Despite pentoxifylline's use for over 30 years, only a few clinically significant cases of liver injury have been associated with it, and the clinical evidence for these cases is not entirely conclusive. However, the pentoxifylline product information lists adverse reactions such as hepatitis, jaundice, cholestasis, and elevated liver enzymes. In the reported cases, the onset time was 3 to 4 weeks, and the pattern of elevated liver enzymes was distinctly cholestatic (Case 1). No autoimmune or immune hypersensitivity features were observed. The injury is self-limiting, and there have been no reports of acute liver failure, chronic hepatitis, or bile duct disappearance syndrome associated with pentoxifylline treatment. Furthermore, pentoxifylline has been evaluated for the treatment of various liver diseases, including acute alcoholic hepatitis and cirrhosis, non-alcoholic fatty liver disease, and autoimmune liver disease, but with mixed results. In several small controlled trials of severe acute alcoholic hepatitis, pentoxifylline treatment was associated with a significant reduction in short-term mortality and the incidence of hepatorenal syndrome. However, in large, well-controlled trials of alcoholic fatty liver disease, pentoxifylline, with or without corticosteroids, had no effect on short- or long-term mortality and little or no effect on the incidence of renal failure. Pentoxifylline has also been reported to improve serum transaminase levels and liver histology in adult patients with non-alcoholic steatohepatitis (NASH), but these findings have not been validated in larger randomized controlled trials. However, all studies have found pentoxifylline to be well-tolerated in patients with liver disease and no evidence of hepatotoxicity. Probability Score: D (Possibly a rare cause of clinically significant liver injury). Effects during Pregnancy and Lactation ◉ Overview of Use During Lactation Limited data suggest that pentoxifylline is rarely excreted into breast milk. No adverse effects are expected on breastfed infants, especially those older than 2 months.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
Pentoxothecobalaine binds to approximately 45% of the erythrocyte membrane.

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1. Acute toxicity: The median lethal dose (LD50) of pentoxifylline in rats is approximately 2000 mg/kg (oral) and the median lethal dose (LD50) in mice is approximately 1000 mg/kg (intraperitoneal injection) [2]
2. Chronic toxicity: In long-term clinical use (600-1200 mg/day for several weeks to several months), pentoxifylline was well tolerated, and no significant histopathological changes were observed in the liver, kidneys, heart, brain or other major organs [2]
3. Adverse reactions: Gastrointestinal symptoms (nausea, vomiting, diarrhea) are the most common adverse reactions, occurring in approximately 3% of patients; these symptoms are mild and usually do not require discontinuation of the drug [1,2]
4. Drug Interactions: Pentoxobromine does not significantly interact with commonly used drugs such as anticoagulants (e.g., warfarin), antihypertensive drugs (e.g., beta-blockers), and lipid-lowering drugs (e.g., statins); at therapeutic doses, it does not inhibit or induce the activity of major CYP450 isoenzymes [2]. 5. Plasma Protein Binding: As described in the ADME section, pentoxobromine has a plasma protein binding rate of approximately 98% in humans and does not significantly displace other drugs that bind to plasma proteins [2].

[1]. Pentoxifylline and its applications in dermatology. Indian Dermatol Online J. 2014 Oct-Dec; 5(4): 510–516.

[2]. Pentoxifylline. A review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic efficacy. Drugs. 1987 Jul;34(1):50-97.

[3]. Synergistic promoting effects of pentoxifylline and simvastatin on the apoptosis of triple-negative MDA-MB-231 breast cancer cells. Int J Oncol. 2018 Apr;52(4):1246-1254.

[4]. Effect of Pentoxifylline on Ischemia- induced Brain Damage and Spatial Memory Impairment in Rat. Iran J Basic Med Sci. 2012 Sep-Oct; 15(5): 1083-1090.

Pharmacodynamics
Pentoxobromine is a synthetic dimethylxanthine derivative with a structure similar to theophylline and caffeine. It possesses hemorheological, antioxidant, and anti-inflammatory properties and has traditionally been used to treat peripheral artery disease (PAD). In PAD patients with comorbid cerebrovascular and coronary artery disease, pentoxobromine treatment has occasionally caused angina, arrhythmias, and hypotension. When used in combination with warfarin, prothrombin time should be monitored more frequently. Furthermore, patients with bleeding risk factors (e.g., retinal hemorrhage, peptic ulcer, and recent surgery) should be monitored regularly for signs of bleeding.

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1. Pentoxobromine is a methylxanthine derivative with hemorheological, anti-inflammatory, and vasoactive effects [1,2]
2. The main mechanisms of action of pentoxobromine include increasing erythrocyte deformability, reducing blood viscosity, inhibiting platelet aggregation and thrombus formation, inhibiting the production of pro-inflammatory cytokines (TNF-α, IL-1β) and activation of the NF-κB signaling pathway, and activating the ERK1/2-AKT signaling pathway [1,2,3]
3. Dermatological applications: Pentoxobromine is a safe and cost-effective drug that can be used to treat leg ulcers, psoriasis, etc. Scleroderma and other skin diseases can be used alone or in combination with other drugs (e.g., corticosteroids for the treatment of psoriasis)[1]
4. Clinical indications: Pentoxobromine is approved for the treatment of peripheral vascular diseases (such as intermittent claudication) and chronic cerebrovascular diseases; preliminary studies have shown that pentoxobromine has potential efficacy in the treatment of sickle cell disease vascular occlusion crisis, hearing impairment, ocular circulatory disorders, altitude sickness, asthenospermia and triple-negative breast cancer (in combination with simvastatin)[2,3]
5. Neuroprotective effects: Pentoxobromine has a protective effect on cognitive function in a rat model of transient global cerebral ischemia, but has no significant protective effect on CA1 pyramidal cells in the hippocampus[4]
6. Dosage forms and dosage: Pentoxobromine is available in two oral dosage forms: regular tablets and extended-release tablets; the recommended daily dose for adults is 600-1200 mg, divided into three doses (200-400 mg each time, three times a day)[2]

C13H18N4O3

278.30702

278.137

6493-05-6

Pentoxifylline-d6;1185878-98-1;Pentoxifylline-d5;1185995-18-9

4740

White to off-white solid powder

1.3±0.1 g/cm3

531.3±56.0 °C at 760 mmHg

98-100°C

275.1±31.8 °C

0.0±1.4 mmHg at 25°C

1.621

0.32

0

4

5

20

426

0

BYPFEZZEUUWMEJ-UHFFFAOYSA-N

InChI=1S/C13H18N4O3/c1-9(18)6-4-5-7-17-12(19)10-11(14-8-15(10)2)16(3)13(17)20/h8H,4-7H2,1-3H3

1,2,3,6-Tetrahydro-3,7-dimethyl-1-(5-oxohexyl)-2,6-purindion

Dimethyloxohexylxanthine; EHT-0202, EHT0202, EHT 0202; BL 191, BL191, BL-191; Oxpentifylline, Pentoxifilina, Theobromine, Trental, Vazofirin, Etazolate

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)

H2O : ~93.3 mg/mL (~335.24 mM)
DMSO : ≥ 2.8 mg/mL (~10.06 mM)

Solubility in Formulation 1: 110 mg/mL (395.24 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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