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Penicillin G

C16H18N2O4S organic

Properties

StateSolid (white crystalline powder)
ColorWhite
SolubilityFreely soluble as the sodium or potassium salt; the free acid is poorly water-soluble
Melting Point214 °C (decomposes)
Boiling PointDecomposes before boiling

About Penicillin G

Penicillin G (benzylpenicillin) is the original beta-lactam antibiotic, formula C16H18N2O4S, molar mass 334.39 g/mol. The structure is a fused bicyclic system: a five-membered thiazolidine ring sharing an edge with the strained four-membered beta-lactam, with a phenylacetamide side chain off the alpha carbon. Alexander Fleming noticed it in 1928 when a Penicillium notatum spore landed on a Staphylococcus plate at St Mary's Hospital and cleared a zone around itself. He published, the work sat dormant for a decade, then Howard Florey, Ernst Chain, and Norman Heatley at Oxford industrialized the production during 1940-43 — the deep-tank fermentation process that scaled up in Peoria, Illinois turned penicillin from a laboratory curiosity into the antibiotic that saved Allied troops from wound sepsis at Normandy. Mechanism: penicillin G mimics the D-Ala-D-Ala terminal dipeptide of the bacterial peptidoglycan precursor and acylates the active-site serine of the transpeptidase enzymes (penicillin-binding proteins, PBPs) that cross-link the cell wall. The acyl-enzyme is essentially irreversible because the strained beta-lactam opens to a stable amide. Without cross-linked peptidoglycan, the cell wall fails under turgor pressure and the bacterium lyses. Pen G is most active against Gram-positive cocci (Streptococcus pyogenes, S. pneumoniae, viridans streptococci), Treponema pallidum (syphilis), and Neisseria meningitidis. Resistance is overwhelmingly through bacterial beta-lactamases that hydrolyze the beta-lactam ring before it can reach the PBP — which is why we now have beta-lactamase-stable derivatives (methicillin, oxacillin) and beta-lactamase inhibitor combinations (amoxicillin/clavulanate, piperacillin/tazobactam).

Where you'll encounter it

If you've ever been diagnosed with strep throat in a clinic and gotten an IM shot in the gluteus, that thick white suspension was benzathine penicillin G — a poorly soluble depot form that releases active drug over 2-4 weeks, which is also the WHO-recommended single-dose treatment for primary syphilis worldwide. Microbiology students still grow Penicillium chrysogenum (the high-yielding strain that replaced notatum) in surface culture to demonstrate the historical fermentation. Industrial penicillin G production now runs around 70,000 tonnes per year from optimized P. chrysogenum strains in 200,000-liter fed-batch bioreactors, with most of it converted to 6-aminopenicillanic acid (6-APA) by penicillin acylase, then re-acylated to make ampicillin, amoxicillin, and the rest of the semi-synthetic penicillin family. Pharmaceutical chemists use 6-APA the way organic chemists use cyclopentadiene — a versatile platform.

Common Uses

  • Treatment of choice for syphilis (single IM dose of benzathine penicillin G)
  • First-line therapy for streptococcal pharyngitis, scarlet fever, and rheumatic fever prophylaxis
  • IV penicillin G for bacterial endocarditis, meningococcal meningitis, and gas gangrene
  • Industrial substrate for enzymatic conversion to 6-APA, the precursor of all semi-synthetic penicillins
  • Teaching example for the discovery of antibiotics and bacterial resistance mechanisms

Safety Information

GHS: H317 (skin sensitizer Category 1), H334 (may cause respiratory sensitization). True IgE-mediated penicillin allergy occurs in about 0.5-2 percent of patients exposed; anaphylaxis is rare (about 1 in 10,000 doses) but can be fatal. Allergy history must be verified before every administration. Self-reported penicillin allergy is the most common drug allergy in medical records but is incorrect about 90 percent of the time, which has driven the current push for formal penicillin allergy de-labeling programs. Side effects of therapeutic dosing include rash, diarrhea, and Jarisch-Herxheimer reactions when treating syphilis. Massive IV doses can cause seizures, particularly in renal impairment.

This safety summary is for educational reference only and may not be complete. It is not a substitute for Safety Data Sheets (SDS), medical advice, or professional chemical safety guidance. Always consult appropriate SDS and qualified professionals before handling chemicals.

Constituent Elements

Frequently Asked Questions

What is the molar mass of penicillin G?
The molar mass of penicillin G (C16H18N2O4S) is 334.39 g/mol from 16 carbon (192.176) + 18 hydrogen (18.144) + 2 nitrogen (28.014) + 4 oxygen (63.996) + 1 sulfur (32.06). Clinical doses are usually quoted in international units rather than mg — 1 million units corresponds to about 600 mg of the sodium salt — a legacy of when penicillin potency had to be measured by bioassay before the molecular weight was confirmed.
How does penicillin kill bacteria?
Penicillin's beta-lactam ring is shaped like the D-Ala-D-Ala dipeptide that the bacterial transpeptidase (a penicillin-binding protein, PBP) recognizes during cell-wall cross-linking. The active-site serine of the PBP attacks the strained beta-lactam carbonyl, opens the ring, and forms a stable acyl-enzyme — irreversibly inactivating that PBP. Without cross-links between peptidoglycan strands, the cell wall can't withstand the 5-25 atm internal turgor pressure of a growing bacterium, and the cell lyses. The drug is bactericidal only against actively dividing bacteria for this reason.
How do bacteria become resistant to penicillin?
Three main routes. First and most common: bacterial beta-lactamases — secreted enzymes that hydrolyze the beta-lactam ring before it ever reaches a PBP. Most Staphylococcus aureus strains acquired this within years of penicillin's introduction. Second: PBP modification — methicillin-resistant S. aureus (MRSA) carries the mecA gene encoding PBP2a, which has low affinity for all beta-lactams. Third: reduced permeability and active efflux, particularly in Gram-negatives where the outer membrane already excludes large hydrophilic molecules and porin loss makes it worse. Beta-lactamase inhibitors (clavulanate, sulbactam, tazobactam) are the standard countermeasure for the first mechanism.