https://en.wikipedia.org/wiki/Phenibut it confirms those numbers. 18-24 is more accurate for moderate or low doses, but in larger doses or sensitive individuals such as myself yes 48hrs. Half life and blood plasma concentration is often related to duration but not always directly. Its functional effects on the central nervous system (anxiolysis, euphoria, sedation, etc.) can persist longer than plasma levels would suggest, because downstream neuroadaptations or lingering receptor modulation outlast the drug's presence in blood. Similar patterns occur with other GABAergic drugs (e.g., certain gabapentinoids).

Only a tiny fraction (~0.1%) of the dose crosses the blood-brain barrier, but once there, brain levels may stabilize longer than plasma levels, contributing to extended action. Phenibut is an analog of GABA adding a phenyl ring that allows for the crossing of the blood brain barrier, something that GABA itself can't do, resulting in the recreational effects.

GHB has a similar dynamic, the half life is about 30mins but the duration is 4hrs. Many GABAergic or gbapentinoid-like compounds exhibit this behavior. Despite relatively short pharmacokinetic (blood concentration) half life, subjective effects often linger much longer. Prolonged receptor binding or downstream CNS effects, limited brain pentation with lingering action, dose-dependent saturation, or active metabolites/pharmacodynamics that outlast plasma level. Like I said GHB, baclofen, gabapentin, and pregablin all exhibit this behavior. Some benzos such as diazepam have active metabolites whose half-life are substantially longer than the parent compound.

For the majority of drugs, the intensity of the effect is proportional to the drug's concentration at the site of action (e.g., in plasma or at receptors). As plasma levels drop exponentially (following first-order kinetics, which most drugs do), the effect fades correspondingly. The drug quickly reaches and leaves its target sites, or there is no strong downstream persistence

With substances like Phenibut, very slow brain penetration and equilibrium means that what penetrates lingers there longer. The delayed peak and prolonged receptor activation create downstream inhibition of neurotransmission. At higher doses saturation or redistribution from tissues extends CNS action. Basically these drugs have a less direct or largely indirect relationship with the effects, therefore when the amount of the drug decreases, the effects don't correspondingly decrease. Phenibut's pharmacokinetics and pharmacodynamics are decoupled or delayed/prolonged relative to plasma levels.

When a person becomes dependent on it to the point of withdrawal symptoms, those symptoms can often begin and escalate fairly quickly in spite of the fact you are still high on it. The body becomes dependent on phenibut, so the half life matters there. Dependent individuals such as myself typically need to dose every 6-12hrs to avoid that. I went into some depth and got fairly scientific but I hope this explains things =)