Final Drug List (Updated)

Penicillin (MOA)

Cell wall synthesis inhibitor → blocks peptidoglycan cross-linking

Penicillin (effect)

Weakens bacterial wall so bacteria burst (osmotic lysis)

Penicillin (use)

Broad bacterial infections (esp. Gram+)

Vancomycin (MOA)

Cell wall synthesis inhibitor → binds D-Ala-D-Ala precursors

Vancomycin (effect)

Prevents cell wall building → bacteria cannot survive

Vancomycin (use)

C. difficile (oral works in gut), MRSA (IV)

Clindamycin (MOA)

50S ribosome inhibitor → blocks protein synthesis

Clindamycin (effect)

Stops bacterial protein production (esp anaerobes + Gram+)

Clindamycin (use)

Skin, dental, anaerobic infections; toxoplasmosis alternative

Fidaxomicin (MOA)

RNA polymerase inhibitor → blocks transcription

Fidaxomicin (effect)

Stops bacterial mRNA production → very targeted gut action

Fidaxomicin (use)

C. difficile (low relapse due to microbiome sparing)

Metronidazole (MOA)

Prodrug → activated in anaerobes → causes DNA damage

Metronidazole (effect)

DNA strand breakage in oxygen-free environments

Metronidazole (use)

Anaerobic infections, C. difficile, protozoa

Rifamycin (MOA)

Inhibits bacterial RNA polymerase

Rifamycin (effect)

Blocks transcription → no mRNA → no proteins

Rifamycin (use)

TB + bacterial infections (esp gut prophylaxis variants)

Amphotericin B (MOA)

Polyene that binds ergosterol in fungal membrane

Amphotericin B (effect)

Creates membrane pores → leaks ions → fungal cell death

Amphotericin B (use)

Severe systemic fungal infections, cryptococcosis

Flucytosine (MOA)

Antimetabolite → converted into 5-FU inside fungus

Flucytosine (effect)

Blocks DNA + RNA synthesis in fungal cells

Flucytosine (use)

Cryptococcal meningitis (always combo therapy)

Azoles (MOA)

Inhibit ergosterol synthesis (block fungal membrane production)

Azoles (effect)

Fungal membranes become defective → growth stops

Azoles (use)

Candidiasis, broad systemic fungal infections

Echinocandins (MOA)

Inhibit β-glucan cell wall synthesis

Echinocandins (effect)

Weak fungal cell wall → osmotic rupture

Echinocandins (use)

Candida + invasive fungal infections

Polyenes (MOA)

Bind ergosterol → disrupt fungal membrane integrity

Polyenes (effect)

Membrane becomes leaky → cell contents leak out

Polyenes (use)

Systemic fungal infections

Terbinafine (MOA)

Inhibits squalene epoxidase → blocks ergosterol synthesis

Terbinafine (effect)

Toxic buildup of squalene + weak membrane formation

Terbinafine (use)

Dermatophytes (tinea infections: skin, nails, hair)

Fluconazole (MOA)

Azole → inhibits ergosterol synthesis enzyme (14-α demethylase)

Fluconazole (effect)

Disrupts fungal membrane formation → growth inhibition

Fluconazole (use)

Candida infections (systemic + mucosal)

Ciclopirox (MOA)

Disrupts fungal enzyme systems + metal-dependent processes

Ciclopirox (effect)

Metabolic shutdown in fungal cells

Ciclopirox (use)

Topical skin and nail fungal infections

Miltefosine (MOA)

Disrupts membrane lipids + interferes with cell signaling

Miltefosine (effect)

Membrane instability + metabolic collapse

Miltefosine (use)

Severe protozoal infections (Leishmania)

Olorofim (MOA)

Inhibits dihydroorotate dehydrogenase (pyrimidine synthesis)

Olorofim (effect)

No DNA building blocks → fungal growth stops

Olorofim (use)

Resistant mold infections

Haloprogin (MOA)

Topical antifungal → disrupts fungal membrane integrity

Haloprogin (effect)

Damages fungal cell membrane → leakage and death

Haloprogin (use)

Superficial skin fungal infections (older drug)

Pyrimethamine (MOA)

Inhibits dihydrofolate reductase → blocks folate pathway

Pyrimethamine (effect)

No folate → no DNA synthesis → parasite cannot replicate

Pyrimethamine (use)

Toxoplasmosis

Sulfadiazine (MOA)

Inhibits early folate synthesis (PABA pathway blocker)

Sulfadiazine (effect)

Prevents folate production → synergistic DNA suppression

Sulfadiazine (use)

Toxoplasmosis (used with pyrimethamine)

Folinic acid (MOA)

Rescues host cells by bypassing folate blockade

Folinic acid (effect)

Protects human DNA synthesis from drug toxicity

Folinic acid (use)

Support therapy in toxoplasmosis treatment

Oseltamivir (MOA)

Neuraminidase inhibitor → blocks viral release

Oseltamivir (effect)

Virus cannot exit infected cell → limits spread

Oseltamivir (use)

Influenza A and B

Zanamivir (MOA)

Neuraminidase inhibitor (inhaled form)

Zanamivir (effect)

Prevents viral release from respiratory cells

Zanamivir (use)

Influenza A and B

Baloxavir marboxil (MOA)

Inhibits viral mRNA cap-dependent endonuclease

Baloxavir marboxil (effect)

Stops viral protein synthesis early

Baloxavir marboxil (use)

Influenza (single-dose treatment)

Amantadine (MOA)

Blocks viral uncoating (M2 ion channel inhibitor)

Amantadine (effect)

Virus cannot release RNA into host cell

Amantadine (use)

Influenza A (older resistance-limited use)

Rimantadine (MOA)

M2 ion channel inhibitor → blocks viral uncoating

Rimantadine (effect)

Prevents viral genome release in host cell

Rimantadine (use)

Influenza A (rarely used now)