Learn / Metabolism

Metabolic pathways

Every FMK pathway as a clickable map. Pick one pathway to hammer it — next step, enzyme, regulator, cofactor, and the facts that get tested (NADPH and who needs it, rate-limiting steps, deficiencies) — or set it to all pathways for a mixed drill. Every answer says which enzyme and which pathway.

Pathway

Purine synthesis & salvage · Cytosol — de novo mainly liver; salvage matters most in brain, marrow and RBCs. Enzymes sit beside the arrows; a ★ marks the rate-limiting step. The map scrolls inside its panel.

Zoom

Purine synthesis & salvage

5-Phosphoribosylamine

Made from PRPP by Glutamine:PRPP amidotransferase (GPAT) ★

Glutamine:PRPP amidotransferase (GPAT) ★ rate-limiting · irreversible — Purine synthesis & salvage

Cofactors: Glutamine → glutamate

Activated by: PRPP (substrate availability)

Inhibited by: AMP; GMP (end-product feedback)

The committed step of purine biosynthesis. Three layers of control: PRPP supply, end-product inhibition here, branch-specific feedback below.

Condition cards:6-Mercaptopurine (6-MP) →

Becomes IMP via 9 enzymatic steps (4 ATP, 2 × N¹⁰-formyl-THF)

9 enzymatic steps (4 ATP, 2 × N¹⁰-formyl-THF) — Purine synthesis & salvage

Cofactors: N¹⁰-formyl-tetrahydrofolate (two ring-closure steps), Glycine, glutamine, aspartate, CO₂

Inhibited by: Methotrexate (blocks DHFR → no THF regeneration); Sulfonamides (bacterial folate synthesis, PABA analogs)

Folate is the therapeutic target: methotrexate starves rapidly dividing cells (tumour, marrow, gut) of purines. Sulfonamides hit bacterial folate synthesis only — humans eat their folate.

Condition cards:Methotrexate (folate analog) →Sulfonamides (PABA analogs) →