Penicillin G

Penicillin G is narrow spectrum antibiotic used to treat infections caused by susceptible bacteria. It is a natural penicillin antibiotic that is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms.

Natural penicillins are considered the drugs of choice for several infections caused by susceptible gram positive aerobic organisms, such as Streptococcus pneumoniae, groups A, B, C and G streptococci, nonenterococcal group D streptococci, viridans group streptococci, and non-penicillinase producing staphylococcus. Aminoglycosides may be added for synergy against group B streptococcus (S. agalactiae), S. viridans, and Enterococcus faecalis. The natural penicillins may also be used as first or second line agents against susceptible gram positive aerobic bacilli such as Bacillus anthracis, Corynebacterium diphtheriae, and Erysipelothrix rhusiopathiae. Natural penicillins have limited activity against gram negative organisms; however, they may be used in some cases to treat infections caused by Neisseria meningitidis and Pasteurella. They are not generally used to treat anaerobic infections. Resistance patterns, susceptibility and treatment guidelines vary across regions.

The name "penicillin" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Penicillin G has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of penicillin G results from the inhibition of cell wall synthesis and is mediated through penicillin G binding to penicillin binding proteins (PBPs). Penicillin G is stable against hydrolysis by a variety of b-lactamases, including penicillinases, and cephalosporinases and extended spectrum b-lactamases.

Therapeutic use

For use in the treatment of severe infections caused by penicillin G-susceptible microorganisms when rapid and high penicillin levels are required such as in the treatment of septicemia, meningitis, pericarditis, endocarditis and severe pneumonia.

Dosage and Administration

Penicillin G is destroyed by acid in the stomach, and absorption after oral administration is variable. All Pen G preparations can be injected
IM, and its two highly soluble salts can also be given i.v. The usual route of administration is by intravenous injection. However, IM administration may be preferable in some circumstances, and for patients undergoing continuous ambulatory peritoneal dialysis (CAPD), Pen G can be administered via the intraperitoneal route in the dialysate. Crystalline Pen G is available as either the sodium or potassium salt of benzylpenicillin, with vials of 0.3, 0.6, 1.2, 3.0, and 6 g available. Recommended doses of Pen G (benzylpenicillin) are summarized in Table 1.

Table 1. Recommended doses for Benzylpenicillin.

Age Dose Comments
Adults 2.4–4.8 g daily in four divided doses Can be increased to six doses in life-threatening infections
Neonate (0-1 week) 50 mg/kg daily in two divided doses Higher doses necessary in life-threatening infections, e.g. meningitis
Neonate (1–4 weeks) 75 mg/kg daily in three divided doses As above
Child  (1 month to 12 years) 100 mg/kgdaily in four divided doses  As above

Crystalline Pen G is usually administered every 4–6 hours, but intervals of 2–3 hours between doses may be necessary in severe infections. A common adult dosage is 0.6 g i.m. or i.v. every 4–6 hours. For serious infections (e.g. bacterial meningitis) higher doses can be given; a common dosage for adults is 1.2–1.8 g 4-hourly. Doses higher than this are usually unnecessary for infections, however severe, caused by Pen G-sensitive organisms, although one exception is neurosyphilis, in which doses up to 2.4 g i.v. 4-hourly may be needed.

Crystalline Pen G may be administered i.v. either by continuous infusion or by intermittent injections or infusions. In emergency treatment of serious infections, an initial bolus injection of Pen G should be given i.v. to achieve a high serum level quickly. This can then be followed by either continuous Pen G infusion or intermittent i.v. injections. Continuous infusion was initially considered the preferred method because of the drug’s rapid renal excretion and the presumed increased hazard of thrombophlebitis with intermittent administration. However, problems may arise if Pen G is added to i.v. fluid bottles. It is unstable in solution at room temperature or even at 4°C. Its activity therefore may be progressively lost, and, furthermore, its degradation products may be more potent antigens than Pen G itself and cause sensitization. 

For renally impaired patients, dose adjustment is recommended as shown in Table 2.

Table 2. Recommended dosage schedule for intermittent i.v. benzylpenicillin therapy for patients with renal failure.

Creatine clearance (ml / min)  Dose (g) Interval (hrs)
125 1.2 or 1.8 2 or 3
60 1.2 4
40 0.9 4
20 0.6 4
10  0.6 6
0 0.3 or 0.6 6 or 8


Oral LD50 in rat is 8900 mk/kg. Neurological adverse reactions, including convulsions, may occur with the attainment of high CSF levels of b-lactams. Neutropenia can occur if high doses are administered consistently for over 2 weeks.

Hypersensitivity reactions

These are common and sensitization is usually the result of previous treatment with a penicillin, but some subjects have had immediate reactions to the drug when first treated. The Pen G molecule may also evoke allergy by acting as a hapten and combining with body proteins to form an antigenic compound. Various derivatives of the penicillin nucleus, 6-APA, often share crosssensitivity, demonstrating that it also plays an important role. It was predicted that all penicillins derived from 6-APA would cross-react in sensitized individuals, but this is not invariable.

The Pen G molecule does not combine readily with protein to produce an antigen, and the actual haptens are various penicillin breakdown products. The most important of these is the penicilloyl derivative, which is formed by breaking of the beta-lactam ring; this may become stably attached to protein via an amino group. This penicilloyl derivative can arise directly from Pen G or through an intermediary, penicillenic acid, which is another penicillin degration product. The conjugate of the penicilloyl derivative with body proteins is commonly called the ‘‘major antigenic determinant’’ [1]. Other penicillin degradation products, such as penicilloic acid, which are also involved in allergy, are grouped together and called ‘‘minor antigenic determinants’’.

The major antigenic determinant cannot be used for skin testing procedures because it is itself a potent sensitizing agent. When the penicilloyl derivative is conjugated with polymerized lysine, penicilloyl-polylysine (PPL) results, which appears to be much safer as a skin test reagent.

Pen G can become more allergenic after a period in solution, either because it is degraded to more allergenic substances or because of the
formation of high-molecular-weight Pen G polymers [2]. It is therefore always wise to use freshly prepared Pen G solutions.
Penicillin hypersensitivity may be broadly divided into the following four types:

1. Anaphylactic reactions.

These are type 1 hypersensitivity reactions occurring in previously sensitized patients. These are rare, but they may result in death within minutes. Features are nausea, vomiting, abdominal pain, pallor, tachycardia, severe dyspnea due to bronchospasm, rigors, loss of consciousness, and peripheral circulatory failure due to vasodilation and loss of plasma volume into the tissues. Acute urticaria and angioneurotic edema, which may affect the larynx, can also occur [3].

Anaphylactic reactions are largely mediated by IgE (reaginic) antibodies, but certain IgG subclass antibodies may also play a part [4]. In large-scale surveys, anaphylactic reactions have occurred in approximately 0.05% of Pen G-treated patients [1,5-6]. Thus, anaphylaxis to Pen G has been estimated to occur in about 1–5 per 10,000 patients treated, with fatalities in as many as 1–5 of 100,000 treated patients [6]. Thus, about 10% of anaphylactic reactions may be fatal [7]. Parenteral Pen G accounts for nearly all cases of anaphylaxis, but there are occasional reports following the use of oral potassium Pen G [8].

2. Serum sickness (late reactions).

These are type 4 T-cell mediated reactions and have occurred in approximately 2% of patients treated with Pen G [7]. They usually appear 7–10 days after primary administration of Pen G. They are produced by circulating immune complexes, the formation of which is possible because intravascular antigen is still present when antibody is first produced [4]. Serum sickness is characterized by fever, malaise, urticaria, joint pains, lymphadenopathy, and occasionally angioneurotic edema. Erythema nodosum is a less common manifestation. Exfoliative dermatitis (which may be serious or even fatal) and Stevens–Johnson syndrome may rarely occur. Drug fever may be the sole manifestation of Pen G-induced serum sickness [9]. However, other authors consider that the mechanisms by which drugs induce fever have not been well delineated and that this reaction may not have an allergic basis [10]. Serum sickness is usually not serious and it subsides when Pen G is withdrawn. Antihistamines are helpful but in severe cases corticosteroids are necessary.

3. Contact dermatitis.

This results from topical Pen G application or exposure to Pen G aerosol; it is an occupational disease of nurses and other healthcare workers.

4. Local reactions.

Swelling and redness at the site of Pen G injections may occur.

Jarisch–Herxheimer reaction

Jarisch–Herxheimer reaction may be evoked when patients with syphilis are treated with Pen G. It was initially thought to be due to release of endotoxins (lipopolysaccharides) from large numbers of killed treponemas [11]. This was not borne out by studies in animals. Other possible causes were considered to be the formation of immune complexes with treponemal antigens or the release of a nonendotoxin pyrogen from Treponema pallidum [12]. However, it now appears that the reaction is mediated by the action of cytokines released into the circulation [13]. The reaction usually occurs 6–8 hours after commencement of Pen G and subsides within 12–24 hours. Features include malaise, chills, fever, sore throat, myalgia, headache, and tachycardia; there may be an exacerbation of existing syphilitic lesions, for example flaring of the rash of secondary syphilis [11,14]. Reactions in early syphilis are unpleasant but not serious. In late cardiovascular or neurosyphilis, serious reactions, although rare, are possible due to aggravation of local lesions. Patients with late cardiovascular disease may die during a reaction, and those with cerebral syphilis may develop increased mental disturbance [14].

The Jarish–Herxheimer reaction may occur in about 50% of patients treated with Pen G for primary syphilis, 75% of those with secondary
syphilis, and 30% of those with neurosyphilis [11].

Jarisch–Herxheimer reactions occur when certain other infections are treated by Pen G. They are frequent in leptospirosis and result in fever, hypotension, and precipitation or aggravation of the features of the disease. The reaction may even precipitate the need for hemodialysis and adult respiratory distress syndrome [15-16]. It may follow the use of Pen G for the treatment of yaws, rat bite fever, anthrax, and, rarely, meningococcal meningitis [17].

A Jarisch–Herxheimer reaction can complicate the treatment of some infections by other antibiotics. A severe form may be provoked by tetracyclines in louse-borne relapsing fever, which may be fatal [14].


Interstitial nephritis, which occurs with many antibiotics, particularly methicillin, can complicate i.v. administration of large doses of Pen G (12–36 g daily) [18-19]. This usually ensues after about 8 days’ treatment and is manifested by fever, eosinophilia, occasional rashes, albuminuria, and a rise in blood urea. Renal biopsy shows interstitial nephritis without glomerular abnormalities or arteritis. Most patients recover when Pen G is stopped. A hypersensitivity mechanism is probably involved. There is no evidence that patients with renal impairment are more likely than patients with normal renal function to develop this complication when treated with appropriately adjusted doses of Pen G. If too high doses are used, renal function may be aggravated [20].

Milder forms of Pen G hypersensitivity nephritis may present with features of dysuria, pyuria, proteinuria, and eosinophilia, suggesting a urinary tract infection, there usually being no azotemia. It rapidly resolves when Pen G is withdrawn, but promptly recurs on readministration of the drug [21].

Rarely, renal disease characterized by glomerulonephritis or periarteritis has been associated with the administration of relatively low doses of Pen G. The causal role of Pen G in these cases is doubtful [18].

Hemolytic anemia

This uncommon complication may happen when i.v. Pen G in a dose usually greater than 6 g/day is given to patients who have previously received large doses of the drug [22]. Characteristic of hemolysis, the hemoglobin level falls and the reticulocyte count rises. Pen G-induced hemolytic anemia is of the hapten type, i.e. the antibody produced is directed to the drug (hapten). A strongly positive direct antiglobulin reaction (Coombs test) is the main diagnostic feature, which is due to induced IgG antibody reacting with Pen G-coated red cells [23-24]. Erythrocytes not coated with Pen G may also be destroyed because they may bind activated complement components and thereby be susceptible to premature destruction by the reticuloendothelial system [25].

Pen G-induced hemolytic anemia should be suspected in patients who develop anemia while receiving high doses of Pen G. Patients with severe infections such as bacterial endocarditis often develop anemia due to infection and the hemolytic component may be overlooked. On withdrawing Pen G the hemoglobin value usually rises quickly and the direct antiglobulin test becomes negative in one to three months. In most cases Pen G-induced hemolysis is not very severe; occasionally rapid intravascular hemolysis followed by renal failure or even circulatory collapse and death may ensue [26].

IgG antibody to Pen G often cross-reacts with red cells sensitized with the semisynthetic penicillins and cephalosporins, so that these drugs are not safe alternatives [22]. It is much less common for Pen G administered in ordinary therapeutic doses to cause hemolytic anemia, but it has been reported [27]. In these cases, IgG antibody cannot be detected but an IgM antibody is present [28]. Pen G has been suggested as a possible cause of microangiopathic hemolytic syndrome (thrombotic thrombocytopenic purpura) in one patient [29].

Other hematologic side-effects

Pen G, in large doses, can rarely cause pancytopenia due to apparent blockade of the release of mature cells from the bone marrow [30]. Severe neutropenia, usually resulting from the use of high doses of Pen G i.v. for several weeks, is another complication which usually resolves when Pen G is stopped [31-32]. This neutropenia appears to be dose related. Neutropenia is a common complication when Pen G in a dose of 18 g i.v. is used to treat bacterial endocarditis, whereas this complication is uncommon with a dose of 12 g i.v. cloxacillin daily [33]. Patients with initial low counts of neutrophils were found to have an increased risk of developing neutropenia.

Pre-existing liver disease also predisposes patients to Pen G-induced leukopenia. Pen G and other beta-lactam antibiotics, when administered in usually recommended dosages, can induce leukopenia in these patients. The more severe the hepatic dysfunction, the greater the risk. Doses of beta-lactams may need to be reduced in these patients [34].

When Pen G-induced neutropenia resolves after cessation of the drug, it may recur if another beta-lactam is used. In one case neutropenia recurred when cefuroxime was given in high doses i.v. as a substitute for Pen G in the treatment of gonococcal endocarditis. The neutropenia resolved when i.v. erythromycin was substituted for cefuroxime [35]. Severe neutropenia is a well-known complication of high-dose therapy with most beta-lactam antibiotics. Secondary infection related to this neutropenia has been observed in only a few cases and no fatalities have been reported. However, therapy with high doses of beta-lactams in granulocytopenic patients receiving cytotoxic therapy simultaneously may prolong the episode of granulocytopenia. It is not yet known how this effect can be recognized clinically and whether this may have an adverse effect on therapeutic outcome [36].

If administered in large doses of 6 g daily to uremic patients, or 24 g daily to those with normal renal function, Pen G can induce coagulation disorders. These may appear soon after Pen G administration is commenced and persist for about 4 days after it is stopped. Factors involved are platelet dysfunction, disturbed conversion of fibrinogen to fibrin and increased antithrombin III activity [37-38].

Pen G therapy can also be associated with the development of acquired inhibitors of blood coagulation, particularly blocking inhibitors. These are proteins but not necessarily antibodies which can interfere with many aspects of the coagulation reaction, but they are rarely, if ever, associated with overt bleeding. The prothrombin time is normal, but the activated partial thromboplastin time is usually prolonged.

Uncommonly, Pen G hypersensitivity may be associated with the presence of specific clotting factor inhibitors which inactivate single factors. Inhibitors specifically directed against factors V, VIII, IX, and XI have been described, factor VIII inhibitors being the most common. These factor inhibitors appear to be antibodies and their presence may be associated with severe bleeding [39].

Cation intoxication

A quantity of 0.625 g of the potassium salt of crystalline Pen G contains 1.5 mEq of potassium ion (0.066 g potassium). If ‘‘massive doses’’ of this preparation are given i.v., potassium intoxication may occur. The sodium salt of Pen G, which contains 1.7 mEq (or 0.039 g sodium) in 0.6 g, is unlikely to cause complications, unless ‘‘massive doses’’ are used in patients with renal or cardiac failure. Pen G probably induces excessive renal potassium loss by direct action on distal renal tubules, thereby producing hypokalemia and metabolic alkalosis. Antibiotics such as Pen G may also cause a redistribution of potassium within the body [40].

Other rare side-effects

Pen G has occasionally been reported as the cause of pericarditis, myocarditis, intestinal hemorrhage, liver necrosis, and gangrene [1]. It may cause hypersensitivity vasculitis [41]. Cholestasis has been reported [42]. It has been tenuously associated with drug-induced lupus syndromes. Pen G therapy can cause eosinophilia and pulmonary infiltration, but this is a rare association compared with that with other chemotherapeutic agents, such as nitrofurantoin and the sulfonamides [43]. Benign intracranial hypertension may occur rarely due to vasculitis caused by Pen G hypersensitivity [44]. One patient who experienced a severe serum sickness following Pen G later developed increased intracranial pressure due to pachymeningitis which responded to corticosteroids [45]. Intravenous Pen G is said to be a rare cause of colicky abdominal pain [46].

Nerve and muscle injury

The danger of sciatic nerve injury from IM Pen G injections in the buttock is well known, and in most hospitals the drug is given in the lateral aspect of the thigh. Muscle necrosis and abscess formation can occur after IM injection, and rarely muscle contractures may be a sequel to repeated IM injections in the thigh.


Serum levels in ten patients with normal renal function, who received an i.v. injection of 3 g of sodium Pen G over a 3- to 5-minute period have been studied [47]. The resulting mean serum concentration after 5 minutes was 400 mg/ml, and after 10 minutes, 273 mg/ml. During the first hour there was a rapid decrease in the serum concentrations (due to both distribution and elimination of the drug), after which the mean serum level was 45 mg/ml. The subsequent fall in serum levels was slower, and presumably this was mainly due to Pen G elimination; at 4 hours the mean serum level was 3.0 mg/ml.

When the same dose of Pen G was administered by continuous infusion over a 6-hour period, 2 hours was required to achieve a serum level of 12–20 mg/ml, which then could be maintained only by the use of a constant-infusion pump. If the infusion was given by an ordinary i.v. drip, large fluctuations of serum levels were observed, despite close supervision.

Bioavailability 15-30%
Protein binding 45-68%
Metabolism 16-30% of intramuscular dose is metabolized to penicilloic acid, an inactive metabolite.

Small amounts of 6-aminopenicillanic acid recovered in the urine. A small percentage of the drug appears to be hydroxylated into one or more active metabolites, which are excreted via urine.

Half-life 0.4–0.9 hours
Cmax (mg/ml)  
tmax (hrs)  
Distribution volume Vd (l/kg) 0.53–0.67 
Clearance 560ml/min
Excretion Kidneys. Nonrenal clearance includes hepatic metabolism and, to a lesser extent, biliary excretion.


Rapidly absorbed following both intramuscular and subcutaneous injection. Initial blood levels following parenteral administration are high but transient. Oral absorption in fasting, healthy humans is only about 15-30% as it is very susceptible to acid-catalyzed hydrolysis.

Immediate high serum levels are attained after rapid i.v. injection of crystalline Pen G. If a dose of 1.2 g is administered intermittently i.v.
every 2 hours, or 1.8 g every 3 hours, a mean serum concentration of approximately 20 mg/ml is attained [48].


Pen G penetrates into bronchial secretions to a modest degree; peak sputum concentrations are only 5–20% of those in serum [49]. Pen G diffuses quite readily into lung empyemas, uncomplicated para-pneumonic effusions [50], and ascitic fluid [51]. Similarly, the drug penetrates well into pericardial and synovial fluids. Pen G easily diffuses into inflamed tissues, where it persists longer than in normal tissues [52]. Pen G concentrations in purulent saliva of patients with bacterial parotitis are considerably higher than in nonpurulent saliva of healthy patients [53]. The drug’s passage into hematomas is quite good [54], but it is poor into noninflamed bone, avascular areas, and abscesses.

Penetration of Pen G into the CSF of patients with noninflamed meninges is poor. Serial CSF Pen G concentrations in children with bacterial meningitis who were treated by i.v.have been reported [55] Pen G in a dosage of 0.15 g/kg per day. Mean CSF Pen G concentrations on days 1, 5, and 10 of therapy were 0.8, 0.7, and 0.3 mg/ml, respectively. These decreasing CSF levels correlated with the return of CSF protein concentrations toward normal.

When parenteral Pen G is administered to subjects with normal meninges, CSF Pen G levels are kept low, not only by passive CSF flow into the venous system via the arachnoid villi, but also by an active transport system localized in the choroid plexus, which specifically excretes Pen G and other organic acids from the CSF [55-56]. In patients with meningitis, there is increased vascular permeability, allowing more Pen G to enter the CSF, and also a decreased clearance from the CSF by partial inhibition of the organic acid pump. In normal animals and in those with experimental bacterial meningitis, CSF Pen G levels increase two to three times if probenecid is also given. This increase is greater than can be expected from the associated serum level increase.

Pen G enters erythrocytes. If it is given by a direct i.v. injection followed by a constant Pen G infusion, the red blood cell Pen G concentration equals or exceeds the serum concentration after 2 hours. If Pen G administration is then ceased, the erythrocytic Pen G concentration is only halved in 50–60 minutes, whereas the serum Pen G half-life is 30 minutes. This slower rate of efflux of Pen G from erythrocytes probably helps to maintain high initial drug levels for a longer period [57]. Pen G, unlike antibiotics with good lipid solubility, such as chloramphenicol and rifampicin, penetrates poorly into human polymorphonuclear leukocytes and into enucleated human polymorphonuclear leukocytes (cytoplasts) [58-59]. 


Penicillin G is eliminated by the kidneys. Nonrenal clearance includes hepatic metabolism and, to a lesser extent, biliary excretion.

If renal function is normal, over 70% of an injected dose of Pen G is excreted within 6 hours, mainly as the active drug, and high urinary concentrations are attained. In healthy adults, only about 10% of an injected dose of Pen G is excreted by glomerular filtration, the remainder predominantly by tubular secretion [60]. Animal experiments indicate that this secretion takes place in the proximal tubules, and that a small amount (about 10% of the administered dose) is then reabsorbed in the collecting ducts [61]. After this rapid elimination phase of Pen G, there may follow a slow elimination phase [62]. In human volunteers the serum levels were still approximately 0.01 mg/ml
9 hours after administration of 0.6 g Pen G i.v.. In newborn infants excretion is predominantly by glomerular filtration, because of the immaturity of tubular function at that age [55]; this results in a prolonged Pen G serum half-life.

In patients with impaired renal function, the Pen G serum half-life increases as renal function deteriorates [47], but the drug still disappears from the blood at a significant but reduced rate in anuric patients. Elderly subjects also have a diminished renal tubular secretory ability and are liable to Pen G neurotoxicity, if large doses are given i.v. Renal tubular secretion can be partly blocked by probenecid and, if probenicid is co-administered, Pen G serum concentrations are approximately doubled.

Some active Pen G is eliminated in bile. In animals, the drug is actively secreted into the bile and amounts to about 4.5% of the administered dose. Probenecid may reduce biliary secretion and possibly also interfere with Pen G inactivation in the liver because it significantly prolongs the cloxacillin half-life in anephric patients [63]. Pen G which is not excreted in urine or bile (usually less than 30%)
is inactivated in the liver, producing mainly penicilloic acid [64]. Inactivation of Pen G is more rapid than that of other penicillins, such as ampicillin and carbenicillin, so that in anuric patients the serum half-life of Pen G is only 3 hours, but with ampicillin and carbenicillin it is 7–8 and 15 hours, respectively. Serum levels of Pen G decline very slowly in patients with severe hepatic and renal dysfunction [48].


About 16-30% of an intramuscular dose is metabolized to penicilloic acid, an inactive metabolite. Small amounts of 6-aminopenicillanic acid have been recovered in the urine of patients on penicillin G. A small percentage of the drug appears to be hydroxylated into one or more active metabolites, which are also excreted via urine.

Mechanism of Action

By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, penicillin G inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that penicillin G interferes with an autolysin inhibitor.

Other pharmacological effects


Medicinal Chemistry

CAS number: 61-33-6   EINECS:

Molecular Formula: C16H18N2O4S

Average mass:   334.39 Da

Monoisotopic mass: 334.098727764 Da

Systematic name: (2S,5R,6R)-3,3-dimethyl-7-oxo-6-(2-phenylacetamido)-4-thia-1-azabicyclo[3.2.0]heptane-2-carboxylic acid

SMILES: [H][C@]12SC(C)(C)[C@@H](N1C(=O)[C@H]2NC(=O)CC1=CC=CC=C1)C(O)=O

Std. InChI: 1S/C16H18N2O4S/c1-16(2)12(15(21)22)18-13(20)11(14(18)23-16)17-10(19)8-9-6-4-3-5-7-9/h3-7,11-12,14H,8H2,1-2H3,(H,17,19)(H,21,22)/t11-,12+,14-/m1/s1



Major Impurities:


Melting point: 214-217 °C

Optical rotation:

Solubility: Slightly soluble (210 mg/L)

logP: 1.83

pKa: 2.74 (at 25 °C)



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